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Type 2 Diabetes is the most common type of diabetes that affects 90 to 95 percent of US diabetes population. Insulin is a hormone that is produced by the pancreas that is needed to provide energy by utilizing glucose, protein and synthesis of fat for the body.
The symptoms of Type 2 diabetes include: weight loss, excessive thirst, profuse urination, tingling in the limbs, lethargy, continuous infection, cramps. In India, the diabetes capital of the world, it is one of the biggest killers, the trigger being in the form of heart attacks, stroke and serious infections. The materials contained on this website are provided for general information purposes only and do not constitute medical, legal, financial or other professional advice on any subject matter. The number of cases of diabetes and prediabetes among Americans of all ages and ethnicities continues to increase, according to the National Diabetes Statistics Report, 2014 (based on health data from 2012), released today by the Centers for Disease Control and Prevention.
People with diabetes often use a blood glucose monitoring device to help them maintain healthy glucose levels.
Senior man using glucometer: Maintaining a healthy blood glucose level helps people with diabetes stay healthy. Biographya€?These new numbers are alarming and underscore the need for an increased focus on reducing the burden of diabetes in our country. Biographya€?If we want to reduce the overall burden of diabetes in our nation, we have to focus on preventing diabetes in the first place."a€?The number of people affected by diabetes and prediabetes has increased across all age groups and ethnicities.
Many tests and statistics become important when one is trying to control blood sugar levels.  The A1C test (or hemoglobin A1c test) is recommended every 3 to 6 months. The American Diabetes Association explains that the A1C test gives an idea of how well your diabetes treatment plan is working. A high A1C means that a change must take place to reduce the risk for serious damage that may result from diabetes. Abbott adds that more than 25 million Americans are living with diabetes and several million remain undiagnosed.
Diabetes Management & Supplies offers accredited diabetes education services that can make managing diabetes and other conditions an easier task.
At Diabetes Management & Supplies, we value the part we play on your treatment plan team and realize that winning is promoting good health. So what we have is American Indians with smaller populations, higher incidences of Diabetes than any other ethnic group in the US, and more at risk than everyone else in the US. A Fact of LifeDiabetes maims, robs, and kills the body and takes away the spirit of living.
Nonetheless, in 2002, Diabetes was the 6th leading cause of death in the US — taking 73,249 lives that we know of. High Blood Pressure or Hypertension — Either hypertension or high blood pressure of 130 over 80+ is found in 73% of adults with Diabetes.
Loss of Limbs — The most severe nerve disease can result in amputation of the lower extremities.
Dental Disease — Periodontal (gum) disease is more common in people with Diabetes and twice as common for young adults with Diabetes, compared to young adults without it. Pregnancy — Major birth defects result in 5 to 10% of pregnancies where Diabetes is poorly controlled before conception and during the first trimester.
Chemical Imbalances — Diabetes that is uncontrolled can cause acute, life-threatening events such as bio-chemical imbalances and even coma. The known death rate linked to diabetes among American Indians is 430% higher than the general US population. The Navajo Elders visited by NRC staff and Program Partners in the Thoreau community of New Mexico had many of the above symptoms.
The CDC Arthritis Program recommends self-management education programs and physical activity programs for all people with arthritis. Health care providers can also help people improve their quality-of-life by referring them to chronic disease self-management education programs that address the effects of arthritis and other chronic conditions.
Learn about CDC recommended intervention programs that are proven to improve the quality of life of people with arthritis. Being physically active is an essential part of preventing and managing many chronic conditions, including arthritis, heart disease, diabetes, and obesity. Health care providers can help people overcome arthritis-specific barriers to physical inactivity by providing appropriate advice and referrals to evidence-based physical activity programs that are designed for adults with arthritis. Learn about intervention programs, such as self-management education programs and physical activity programs, that are designed to teach people the skills they need to take charge of their conditions and engage in effective, joint-friendly physical activity.
Being physically active is an important component of heart disease management, but people with heart disease are less likely to comply with physical activity recommendations than those without heart disease. What are the benefits of increased physical activity for people with heart disease and arthritis?
What are the benefits of increased physical activity for people with diabetes and arthritis? Adults with both arthritis and diabetes were 30% more likely to be physically inactive than those with diabetes only, even after adjustment for age, sex, and body mass index (BMI). What can people with arthritis and other chronic conditions do to overcome the challenges of both conditions? People with arthritis and other chronic conditions can participate in interventions programs, such as self-management education programs and physical activity programs, that are designed to teach them the skills they need to take charge of their conditions and engage in effective, joint-friendly physical activity. Science, Technology and Medicine open access publisher.Publish, read and share novel research. Beta-Cell Function and Failure in Type 2 DiabetesSimona Popa1 and Maria Mota1[1] Department of Diabetes, Nutrition and Metabolic Diseases; University of Medicine and Pharmacy, Craiova, Romania1. Australia's health 2014Understanding health & illness Australia's health system How healthy are we? Some physical and mental conditions can occur across the lifespan among all people, while others occur more frequently among certain age or population groups.
The impact of some types of illness can be surprising—for example, mental and behavioural disorders, which are mostly chronic rather than acute, rank only marginally behind cancer, musculoskeletal conditions and cardiovascular disease, in that order, in terms of disease burden in Australasia. This chapter endeavours to highlight the leading causes of ill health in Australia, both physical and mental, and the impact of these illnesses. There has been considerable success in this country in preventing and treating many chronic diseases—for example, through national cancer screening programs that offer better and earlier detection. To ensure a health system is aligned to a country's health challenges, policy makers must be able to compare the effects of different conditions that cause ill-health and premature death.
The most recent global estimates come from the Global Burden of Disease Study 2010, which covered 241 diseases and injuries and 57 risk factors for 187 countries for 1990, 2005 and 2010 (The Lancet 2012). The last national burden of disease analysis that provided estimates for the Australian and Aboriginal and Torres Strait Islander populations was published in 2007, based on 2003 data. What follows is a snapshot of the global study findings for the Australasia region (Australia and New Zealand) published in late 2012.
Non-communicable (largely chronic) diseases accounted for about 85% of the total burden of disease in Australasia in 2010, while injuries accounted for 10%.
The largest contributors to the total burden were cancer (16%), musculoskeletal disorders (15%), cardiovascular diseases (14%) and mental and behavioural disorders (13%). Musculoskeletal disorders contributed 26% and mental and behavioural disorders 23% of the non-fatal burden in 2010.
Of the risk factors considered by the study, dietary risks (accounting for 11% of the total burden), high body mass index (9%) and smoking (8%) were the leading risk factors.
While these risk factors are known to be associated with many diseases, the main conditions affected by these risk factors were cancer, cardiovascular diseases, and diabetes, urogenital, blood and endocrine diseases combined.
A larger fraction of the burden is now caused by ill-health rather than premature death (Figure 4.1).
Cancer (ranked 2 in 1990) and musculoskeletal conditions (ranked 3 in 1990) replaced cardiovascular diseases as the leading contributors to the Australasian total disease burden in 2010. Unintentional injuries (other than transport injuries) replaced transport injuries as the largest contributor to injuries.
For risk factors, dietary risks and smoking were ranked 1 and 3 respectively in both 1990 and 2010. Ischemic heart disease, lung cancer and stroke were the top 3 contributors to the fatal burden in all countries, while low back pain was the top contributor to the non-fatal burden. As a group, dietary risks was the largest risk factor contributor to overall burden in those countries. The Global Burden of Disease Study 2010 is an important source of information for setting global health priorities.
The global study also included conditions and risk factors not experienced in Australia (for example, cholera), while other conditions and risk factors of policy interest to Australia were not included (for example, mesothelioma).
Chronic diseases are the leading cause of illness, disability and death in Australia, accounting for 90% of all deaths in 2011 (AIHW 2011b). Many different illnesses and health conditions can be classified under the broad heading of chronic disease.
To simplify, chronic disease is often discussed in terms of 4 major disease groups—cardiovascular diseases, cancers, chronic obstructive pulmonary disease (COPD) and diabetes, with 4 common behavioural risk factors—smoking, physical inactivity, poor nutrition and harmful use of alcohol. Long common in Australia and other developed countries, illness and death from chronic disease is now becoming widespread in developing countries, as rising incomes, falling food prices and increasing urbanisation lead to global changes in diet, overweight and physical inactivity (AIHW 2012d; WHO 2011).
Because of its personal, social and economic impact, tackling chronic disease and its causes is the biggest health challenge that Australia faces. Chronic diseases can range from mild conditions such as short- or long-sightedness, dental decay and minor hearing loss, to debilitating arthritis and low back pain, and to life-threatening heart disease and cancers.
These chronic diseases have each been the focus of recent surveillance efforts, because of their significant health effects and costs, and because actions can be taken to prevent them (AIHW 2011b). Table 4.1 gives a further indication as to how widespread these diseases are, with their consequent toll on health, their demands on primary health care and their cost. Leaving aside more common chronic conditions such as short- or long-sightedness and hearing problems, Australian Health Survey data for 2011–12 indicate that almost 15% of the population had arthritis, 13% had back problems, 10% hypertensive disease, 10% asthma and 10% depression. GPs report that the most common chronic diseases or conditions they see are hypertension, diabetes and depression, followed by arthritis and lipid disorders, including high blood cholesterol. However, death rates for some chronic diseases appear to have peaked in Australia (Figure 4.2), particularly for cardiovascular disease and some cancers such as lung cancer. Deaths registered in 2009 and earlier are based on the final version of cause of death data; deaths registered in 2010 and 2011 are based on revised and preliminary versions, respectively, and are subject to further revision by the ABS. Since chronic diseases are responsible for the greatest amount of illness and death, it is not surprising that they also cause the greatest burden of disease (Table 4.1). The largest disease groups contributing to the Australasian burden of disease in 2010 were cancer, musculoskeletal disorders, cardiovascular diseases, and mental and behavioural disorders. In addition to the personal and community costs, chronic diseases result in a significant economic burden because of the combined effects of health-care costs and lost productivity from illness and death. This amount is conservative because not all health-care expenditure can be allocated by disease, particularly diseases predominantly managed in primary health care. Although patterns of spending vary by disease group, most health dollars that can be allocated to diseases are spent on admitted patient hospital services, out-of-hospital services, medications, and dental services (see Chapter 2 'How much does Australian spend on health care?' and Figure 2.6). Coronary heart disease has a 40% higher death rate and has demonstrated a lesser rate of decline over time among people living in areas of lowest socioeconomic status compared with those in the highest (AIHW, forthcoming 2014b). The rate of new cases of lung cancer for people living in areas of lowest socioeconomic status was 1.6 times that of people in the highest, which is linked to their higher rates of smoking. People who live in areas of lowest socioeconomic status are also more likely to take part in risky health behaviour, or combinations of behaviours, which can lead to poorer chronic disease outcomes. It is useful to examine how chronic disease occurs across different stages of the life course, because of the strong links between earlier exposures and later health outcomes. Social determinants of health, experienced at different life stages, can also influence the development of chronic diseases, through their effect on biological processes (Lynch & Davey Smith 2005). Coronary heart disease and COPD are leading examples of strong links between several life course risk factors and processes and the later development of chronic disease (see Table 4.2).
The most common chronic diseases or conditions among older Australians are some degree of vision or hearing loss, arthritis or other musculoskeletal problems, and elevated blood pressure or cholesterol levels. Chronic diseases are closely associated with modifiable risk factors such as smoking, physical inactivity, poor nutrition and the harmful use of alcohol.
People often have combinations of risk factors, and as their number of risk factors increase, so does the likelihood of developing certain chronic diseases. A group of risk factors, known collectively as the 'metabolic syndrome', greatly increases the risk of type 2 diabetes.
The cumulative effect of risk factors magnifies the risk, with earlier and more rapid development of a condition, more complications and recurrence, a greater disease burden, and a greater need for management of the condition (AIHW 2012b). A key focus of the Australian health system therefore is the prevention and better management of chronic disease to improve health outcomes.
There would seem to be great potential in an integrated and coordinated approach to chronic disease care using shared prevention, management and treatment strategies.
If left unchecked, trends in chronic disease risk factors—especially physical inactivity and poor nutrition leading to overweight and obesity—combined with a growing and ageing population will lead to increasing numbers of people living with chronic diseases. The growing chronic disease burden will require effective treatment of multiple chronic conditions and catering to complex health-care needs.
The availability of better statistical information on the incidence and prevalence of chronic diseases could benefit future health services planning. Additional data on comorbidity and treatment—including data on primary care, health service use, medications and whether these are being taken correctly, quality of life, and people's ability to carry out their daily lives—will also help in developing a picture of how chronic diseases affect people in Australia and the effectiveness of strategies.
Cancer is a diverse group of several hundred diseases in which some of the body's cells become abnormal and begin to multiply out of control.
In 2010, 116,580 new cases of cancer were diagnosed in Australia (excluding basal and squamous cell carcinoma of the skin—the most common types of non-melanoma skin cancer). The risk of being diagnosed with any cancer before the age of 85 was 1 in 2 for males and 1 in 3 for females. The most commonly diagnosed cancers in 2010 were prostate in males (19,821), bowel (14,860), breast cancer in females (14,181), melanoma of the skin (11,405) and lung (10,296) (Figure 4.3).
The number of new cases of cancer diagnosed in Australia is projected to continue to rise over the next decade and is expected to reach 150,000 in 2020. The most common causes of cancer-related death in 2011 were lung (8,114 deaths), bowel (3,999), prostate in males (3,294), breast in females (2,937) and pancreatic (2,416) cancers. In 2006–2010, people diagnosed with cancer had a 66% chance of surviving for at least 5 years compared with their counterparts in the general population (referred to as 5-year survival, see Glossary).
Five-year survival from all cancers increased over time, from 47% in 1982–1987 to 66% in 2006–2010. The cancers with the largest survival gains were prostate cancer, kidney cancer and non-Hodgkin lymphoma. In 2007, about 1 in 28 living Australians had been diagnosed with cancer at some time in the previous 26 years (referred to as 26-year prevalence, see Glossary). In 2011–12, there were more than 908,700 hospitalisations (see Glossary) for cancer or a cancer-related health service or treatment. There are no national registry data on the stage (severity) of cancer at diagnosis, treatments applied to individual cases of cancer, the frequency of recurrence of cancer after treatment, or the incidence of non-melanoma skin cancers. There have been many successes, and there are many remaining challenges, in cancer control. These changes in the cancer landscape are not universal, and differ greatly by cancer type and population group.
The observed rise in overall cancer incidence can be broadly attributed to advancements in early detection (through organised screening programs and better detection technology), the ageing population and changes in risk factor exposure. The net result of increasing cancer incidence and decreasing overall mortality is more people living with cancer, that is, higher and gradually increasing prevalence due to increased survival in the population. Cancer, also called malignancy, is a term for diseases in which abnormal cells divide without control and can invade nearby tissues.
Cancer cells can also spread to other parts of the body through the blood and lymph systems. In 2008–2009, the total health system expenditure in Australia on neoplasms (including cancer and non-cancerous tumours) was $4,526 million, an increase from $2,894 million in 2000–01, after adjusting for inflation (AIHW 2013). There were 116,580 new cases of cancer in 2010 (excluding non-melanoma skin cancer), a rate of 487 per 100,000 people. The incidence of all cancers combined was 1.4 times as high among males (585 per 100,000) compared with females (406 per 100,000). Mortality from all cancers combined was 1.6 times as high among males (219 per 100,000) compared with females (137 per 100,000). Cancer can develop at any age but around 70% of all cancers are diagnosed in people aged 60 and over.
Deaths from cancer are most common among older people, with more than 80% of all deaths from cancer occurring in people aged 60 and over.
Survival decreased with age: from 86% among people aged 0–39 to 43% among those aged 80 and over. Indigenous Australians were 1.1 times more likely to be diagnosed with cancer in 2004–2008 compared with their non- Indigenous counterparts. Indigenous Australians were 1.5 times more likely to die from cancer in 2007–2011 compared with their non-Indigenous counterparts. Indigenous Australians had lower 5-year relative survival (40%) in 1999–2007 compared with their non-Indigenous counterparts (52%). People living in areas of lower socioeconomic status had a higher incidence of all cancers combined (490 per 100,000) compared with people living in areas of higher relative socioeconomic status (482 per 100,000), in 2004–2008.
People living in areas of lower socioeconomic status had higher mortality from all cancers combined (172 per 100,000) compared with people living in areas of higher relative socioeconomic status (151 per 100,000), in 2006–2010.
People living in areas of lower socioeconomic status had lower 5-year relative survival (63%) compared with people living in areas of higher socioeconomic status (71%), in 2006–2010.
Incidence rates of all cancers combined were higher for Australians living in Inner regional areas (504 per 100,000) than people living in Outer regional (495 per 100,000), Major cities (480 per 100,000) and Remote and Very remote areas (474 per 100,000), in 2004–2008. Mortality rates for all cancers combined were higher for Australians living in Remote and Very remote areas (196 per 100,000) and Outer regional areas (193 per 100,000) than for those living in Major cities (171 per 100,000) and Inner regional areas (185 per 100,000), in 2006–2010.
Five-year survival from all cancers combined was highest among people living in Major cities (67%) compared with Inner regional (66%), Outer regional (65%) and Remote and Very remote areas (63%), in 2006–2010.
In Australia, there are some notable historical trends in cancer incidence, mortality and survival (Figure 4.4).
Data points for 5-year relative survival refer to the final year in each 5- or 6-year at-risk period: 1982–1987, 1988–1993, 1994–1999, 2000–2005, 2006–2010.
Changes in cancer incidence, mortality and survival have been shaped by a wide range of factors, including changes in exposure to the risk factors for cancer, improved primary prevention, advancements in cancer treatment, and for some cancers, earlier detection through organised screening programs (bowel, breast and cervical) and opportunistic testing (prostate) (Armstrong 2013). Changes in exposure to cancer risk factors at the population level can increase or decrease cancer incidence, which in turn may produce a parallel change in cancer mortality, noting the lag in time between exposure and the onset of cancer (Armstrong 2013). Selected cancers strongly influenced by changes in exposure to known and quantifiable risk factors in previous decades include lung and stomach cancers, melanoma of the skin and cervical cancer. The major causes of stomach cancer are the bacterium Helicobacter pylori, poor nutrition and smoking. Chronic infection with the human papillomavirus (HPV ) is the cause of around 70–80% of all cervical cancers (Brotherton 2008). Australia has national population screening programs for 3 cancers—breast, cervical and bowel cancer. These screening programs aim to reduce illness and death from these cancers through early detection of cancer and pre-cancerous abnormalities and effective follow-up treatment. The introduction of the BreastScreen Australia program resulted in an initial rapid increase in the number of breast cancers diagnosed in 1992–1994, followed by a more moderate increasing trend to 2010, accompanied by a steady decline in breast cancer mortality from 1994 (Figure 4.5A).
For more information on cancer screening programs, see Chapter 8 'Cancer screening in Australia'. Deaths registered in 2008 and earlier are based on the final version of cause of death data; deaths registered in 2009 and 2010 are based on revised and preliminary versions, respectively, and are subject to further revision by the ABS.
The solid vertical line at 1991 indicates the introduction of the national screening programs. Broadly, a variety of improvements in cancer treatments are thought to have led to improvements in cancer outcomes, particularly decreasing mortality (improved survival). Note: Projected years 2011 to 2020 based on actual data from 1982 to 2007 (incidence) and 1968 to 2010 (mortality).
The combined effect of several factors—increasing incidence, decreasing mortality in some cancers, high and improving survival for some cancers, earlier diagnosis and detection, and developments in treatment and management of cancer—is a steady increase in the proportion of the population who have been diagnosed with cancer. In 2007, there were around 775,000 Australians alive who had been diagnosed with cancer in the 26 years since incidence data were first collected at a national level (from 1982), accounting for 3.7% of the total Australian population in that year (AIHW 2012b).
This will all mean, now and into the future, major changes in the experience of cancer for some individuals, their families and carers (Hawkins et al. These changes and challenges are being seen now in emerging issues such as the survivorship experience, caring for people with cancer, ageing with cancer, recurrent and multiple primary cancers, and cancer in the presence of other conditions (comorbidity). Survivorship is increasingly recognised as beginning at diagnosis and continuing long after treatment ends.
These longer-term risks, and the associated stressors and reduced quality of life for cancer survivors and their family, friends and caregivers, highlight the importance of follow-up health care and of survivorship as part of the cancer control continuum (Hawkins et al. The increasing size of the population who have had cancer also means a corresponding increase in the number of people caring for someone through cancer diagnosis, treatment and remission, often into old age.
The increasing size of the aged population in Australia is a contributing factor to the projected increase in the number of new cancer cases and cancer-related deaths to 2020. As people survive longer with cancer it will become increasingly important for cancer to be considered in the context of patients' other ongoing health conditions. In 2011, cancer was recorded as the underlying cause in 43,221 deaths, accounting for 29% of all deaths in that year. When cancer was recorded as a cause of death (either underlying or associated), it was the underlying cause in 87% of those deaths. As of 2000, at least 171 million people worldwide suffer from diabetes, which is roughly 2. In 2004, heart disease was noted on 68% of diabetes-related death certificates among people aged 65 years or older.
Type 2 diabetes is typified by high blood sugar levels, that can happen due to an a blend of resistance to the action of insulin and the inability of the pancreas to generate sufficient amounts of insulin.
However in some cases, this condition may just be asymptomatic.It has been seen that Type 2 diabetes affects the more than18 percent of the urban population though its incidence in rural areas is lesser.
People with diabetes are at increased risk of serious health complications including blindness, heart disease, stroke, kidney failure, amputation of toes, feet or legs, and premature death. Diabetes experts say that a person with diabetes should have an A1C level below 7%, or as low as possible without risking dangerously low blood sugars. They said they feel that people with diabetes who can understand and manage their condition can prevent or delay health problems, which may lead to longer and healthier lives. NRC Program Partners often tell our staff that as many as 30% to 35% of the people in their community have Diabetes. It shows that the prevalence of Diabetes among American Indians is in fact higher than for other groups, and that overall, American Indians are 2 to 3 times more likely to have Diabetes than non-Hispanic whites.
Over 60% of lower-limb amputations that are nontrauma-related occur in people with Diabetes.
About one-third of people with Diabetes have severe gum disease and their teeth detach from their gums.


Once other illnesses are acquired, the prognosis is often worse and people are more likely to die from pneumonia or flu, for instance, than are people without Diabetes. Obtaining the fresh meats and fresh produce needed to control diabetes, with limited income and access, is a challenge. People with other chronic conditions, such as heart disease or diabetes, who also have arthritis. High blood pressure is also associated with heart disease, the most common comorbidity among adults with arthritis (shown in Figure 1). These programs teach people skills to take charge of their conditions and engage in effective, joint-friendly physical activity. Prevalence of doctor-diagnosed arthritis and arthritis-attributable activity limitation-United States, 2010a€“2012.
Increasing physical activity (for example, through aerobic exercise or strength training) can benefit people with heart disease and arthritis.
Being physically inactive is an even bigger problem for people with heart disease who also have arthritis (Figure 1). Arthritis as a potential barrier to physical activity among adults with heart disease a€” United States, 2005 and 2007. Being physically inactive is an even bigger problem for people with diabetes who also have arthritis. This means that simply having diabetes and arthritis together increases your likelihood of physical inactivity, regardless of your age, sex, or BMI.
Arthritis as a Potential Barrier to Physical Activity Among Adults with Diabetes a€” United States, 2005 and 2007.
We believe health is one of our greatest gifts and are committed to helping others take control of their health for optimum wellness and longevity. Perspective: emerging evidence for signaling roles of mitochondrial anaplerotic products in insulin secretion. Glucokinase as glucose sensor and metabolic signal generator in pancreatic betacells and hepatocytes. Evidence that glucose can control insulin release independently from its action on ATP-sensitive K+ channels in mouse B cells. Beta-cell deterioration determines the onset and rate of progression of secondary dietary failure in type 2 diabetes mellitus: the 10-year followup of the Belfast Diet Study. An overview of pancreatic beta-cell defects in human type 2 diabetes: Implications for treatment.
Kir6.2 variant E23K increases ATP-sensitive K+ channel activity and is associated with impaired insulin release and enhanced insulin sensitivity in adults with normal glucose tolerance. A candidate type 2 diabetes polymorphism near the HHEX locus affects acute glucose-stimulated insulin release in European populations: results from the EUGENE2 study. The common SLC30A8 Arg325Trp variant is associated with reduced first-phase insulin release in 846 non-diabetic offspring of type 2 diabetes patients – the EUGENE2 study. Single-nucleotide polymorphism rs7754840 of CDKAL1 is associated with impaired insulin secretion in nondiabetic offspring of type 2 diabetic subjects and in a large sample of men with normal glucose tolerance. Variants of CDKAL1 and IGF2BP2 affect first-phase insulin secretion during hyperglycaemic clamps. Quantitative trait analysis of type 2 diabetes susceptibility loci identified from whole genome association studies in the Insulin Resistance Atherosclerosis Family Study. Common variant in MTNR1B associated with increased risk of type 2 diabetes and impaired early insulin secretion. Association of 18 confirmed susceptibility loci for type 2 diabetes with indices of insulin release, proinsulin conversion, and insulin sensitivity in 5,327 nondiabetic Finnishmen. Decreased TCF7L2 protein levels in type 2 diabetes mellitus correlate with downregulation of GIPand GLP-1 receptors and impaired beta- cell function. Impact of polymorphisms in WFS1 on prediabetic phenotypes in a population-based sample of middle-aged people with normal and abnormal glucose regulation.
Association of type 2 diabetes candidate polymorphisms in KCNQ1 with incretin and insulin secretion. A variant in the KCNQ1 gene predicts future type 2 diabetes and mediates impaired insulin secretion. Polymorphisms in the TCF7L2, CDKAL1 and SLC30A8 genes are associated with impaired proinsulin conversion. TCF7L2 polymorphisms modulate proinsulin levels and beta-cell function in a British Europid population.
TCF7L2 controls insulin gene expression and insulin secretion in mature pancreatic beta-cells. TCF-4 mediates cell type-specific regulation of proglucagon gene expression by beta-catenin and glycogen synthase kinase-3beta. Hex homeobox gene-dependent tissue positioning is required for organogenesis of the ventral pancreas.
In vivo expression and functional characterization of the zinc transporter ZnT8 in glucose-induced insulin secretion. Increased glucose sensitivity of both triggering and amplifying pathways of insulin secretion in rat islets cultured for 1 wk in high glucose. Role of ATP production and uncoupling protein-2 in the insulin secretory defect induced by chronic exposure to high glucose or free fatty acids and effects of peroxisome proliferator-activated receptor-gamma inhibition. Role of beta-cell dysfunction, ectopic fat accumulation and insulin resistance in the pathogenesis of type 2 diabetes mellitus. Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol.
Palmitate activates AMPactivated protein kinase and regulates insulin secretion from beta cells. Chronic activation of liver X receptor induces beta-cell apoptosis through hyperactivation of lipogenesis: liver X receptor-mediated lipotoxicity in pancreatic beta-cells. Inhibition of PKCepsilon improves glucose-stimulated insulin secretion and reduces insulin clearance.
Palmitate inhibits insulin gene expression by altering PDX-1 nuclear localization and reducing MafA expression in isolated rat islets of Langerhans.
Palmitate inhibition of insulin gene expression is mediated at the transcriptional level via ceramide synthesis.
Evidence against the involvement of oxidative stress in fatty acid inhibition of insulin secretion. Saturated fatty acids inhibit induction of insulin gene transcription by JNK-mediated phosphorylation of insulin-receptor substrates.
Prolonged exposure to free fatty acids has cytostatic and pro-apoptotic effects on human pancreatic islets: evidence that beta-cell death is caspase mediated, partially dependent on ceramide pathway, and Bcl-2 regulated. Monounsaturated fatty acids prevent the deleterious effects of palmitate and high glucose on human pancreatic beta-cell turnover and function.
Free fatty acid-induced beta-cell defects are dependent on uncoupling protein 2 expression. And some types of ill health have a bigger impact on our society than others in terms of healthy years of life lost due to illness or death—often referred to as burden of disease. Chronic diseases, including cancer which is also featured in this chapter, are the leading cause of ill health and death in Australia, and have been for some decades, now that the impact of communicable diseases has diminished through vaccination and other prevention and treatment practices. But overall, the adverse effects of behavioural and other health risk factors, combined with an ageing population, have led to an increase in their impact on our society. Burden of disease analysis simultaneously compares the non-fatal burden (impact of ill-health) and fatal burden (impact of premature death) of a comprehensive list of diseases and injuries, and quantifies the contribution of various risk factors to the total burden as well as to individual diseases and injuries. To enable global comparability on such a broad scale, the study needed to introduce innovative methods as well as manage limitations in data availability. The AIHW is updating these estimates using the 2010 global burden of disease methodology where possible, with some enhancements to better suit the Australian and Indigenous contexts, and using more recent and detailed Australian data. High body mass index was the second-highest risk factor in 2010, replacing high blood pressure, which was second highest in 1990.
However, it does not provide estimates by population groups—in particular the Aboriginal and Torres Strait Islander population—or at a subnational level (for example, by state and territory, remoteness or socioeconomic classification).
The advent of chronic diseases follows successes in limiting infection and infant deaths during the late 19th and early 20th century. They often coexist, share common risk factors and are increasingly being seen as acting together to determine the health status of individuals. Between them, these 4 disease groups account for three-quarters of all chronic disease deaths.
The worldwide chronic disease 'pandemic' was the subject of a high-level United Nations meeting in 2011, which called for a 25% reduction by 2025 in mortality from chronic diseases among people aged between 30 and 70, adopting the slogan '25 by 25' (Beaglehole et al. A growing understanding that many of these diseases arise from similar underlying causes, have similar features, and share a number of prevention, management and treatment strategies, as well as significant and increasing costs, is challenging us to transform the way in which we respond to chronic disease.
They can result from complex causes, which can include a number of different health risk factors.
These conditions may never be cured completely, so there is generally a need for long-term management.
Analysis of the 2007–08 National Health Survey indicates that one-third of the population (35%, or 7 million people) reported having at least 1 of the following chronic conditions: asthma, type 2 diabetes, coronary heart disease, cerebrovascular disease (largely stroke), arthritis, osteoporosis, COPD, depression or high blood pressure. Since 1980, coronary heart disease (CHD) mortality has declined by 73%, cerebrovascular disease by 69% and all cancers by 17%.
Data for 2010 have not been adjusted for the additional deaths arising from outstanding registrations of deaths in Queensland in 2010.
Cardiovascular diseases (coronary heart disease and stroke), dementia and Alzheimer disease, lung cancer and chronic lower respiratory disease including COPD are the most common underlying causes, together being responsible for 40% of all deaths. The overall burden is measured by the disability-adjusted life year (DALY), which is expressed as the number of years lost due to ill health, disability or early death (see Chapter 4 'Burden of disease').
The 5 leading individual causes of disease burden—heart attack, low back pain, COPD, depression and cerebrovascular disease—accounted for one-quarter of the disease burden.
Estimates based on allocated health-care expenditure indicate that the 4 most expensive disease groups are chronic—cardiovascular diseases, oral health, mental disorders, and musculoskeletal—incurring direct health-care costs of $27 billion in 2008–09. Chronic disease costs would also be far greater if non-health sector costs, such as residential care, were included.
The large cost, in the order of several billions of dollars, is 1 of the key drivers for more efficient and effective ways to prevent, manage and treat chronic disease. They occur more often among Indigenous Australians, for example, and at a much younger age (AIHW 2010).
Survival of people diagnosed with cancer living in the lowest status areas is also lower (AIHW & AACR 2012). In 2011–12, people living in areas of lowest socioeconomic status were 2.3 times as likely to smoke as those living in the highest (ABS 2013a). In 2007–08, 350,000 people (2% of the total population) reported having 4 or more concurrent chronic health conditions out of a list comprising asthma, type 2 diabetes, coronary heart disease, cerebrovascular disease, arthritis, osteoporosis, COPD, depression and high blood pressure. Some diseases, such as asthma and type 1 diabetes, usually begin in childhood or adolescence. Often, adult chronic diseases reflect the cumulative influence of prior physical growth, of reproduction, infection, social mobility and changes in behaviour. Low birthweight babies, for example, are more likely to come from less affluent backgrounds, and low birthweight is associated with increased rates of cardiovascular disease and diabetes later in life.
Many of these risk factors can interact with each other as well as with chronic disease development.
Around 15% of people in the 0–24 age group reported having either asthma, type 2 diabetes, coronary heart disease, cerebrovascular disease, arthritis, osteoporosis, COPD, depression or high blood pressure, in 2007–08.
Yet despite the frequency of chronic disease in later life, two-thirds of older Australians aged 75 and over rate their health as good, very good or excellent.
Modifying these can reduce the risk of developing a chronic condition, leading to large health gains in the population through the reduction of illness and rates of death (see Chapter 8 'Prevention for a healthier future').
These behaviours contribute to the development of biomedical risk factors, including overweight and obesity, high blood pressure, and high cholesterol levels, which in turn lead to chronic disease (see Chapter 5 'Biomedical risk factors' and 'Behavioural risk factors' for further details). For example, males with 5 or more risk factors are 3 times as likely to have COPD as males with 2 or fewer risk factors. In 2010, 38% of current smokers also consumed alcohol at risky levels, compared with only 12% of people who had never smoked (AIHW, forthcoming 2014a).
This risk factor group comprises obesity, impaired fasting blood glucose, raised blood pressure, raised blood triglycerides and reduced HDL cholesterol.
Many common chronic diseases are amenable to preventive measures such as changes in behaviour. Reducing obesity, for example, may prevent diabetes, hypertension, heart disease, and certain types of cancers. Helping people to make good lifestyle choices at all stages of the life course can help to keep them in good health and prevent illness for as long as possible. Developing and implementing new and innovative treatment methods—including coordinated care and chronic disease management plans—holds great promise for future disease management (see Chapter 8 'Primary health care in Australia'). Contribution of chronic disease to the gap in adult mortality between Aboriginal and Torres Strait Islander and other Australians. Multiple causes of death in Australia: an analysis of all natural and selected chronic disease causes of death 1997-2007. The abnormal cells can invade and damage the tissue around them, and spread to other parts of the body, causing further damage and eventually death. Between 1990 and 2010, the age-standardised incidence rate (see Glossary) for total cancers rose by 16%, from 422 new cases per 100,000 people to 488 per 100,000. This increase in the number of new cases, due primarily to population growth and ageing, is expected to be most evident among older populations.
Between 1991 and 2011, the age-standardised mortality rate for all cancers combined fell by 17%, from 210 deaths per 100,000 people to 172 per 100,000.
Among people who had already survived 5 years past their cancer diagnosis, the chance of surviving for at least another 5 years was 91%. Some of the likely reasons for this include better diagnostic methods, earlier detection and improvements in treatment. The cancers with a decline or no improvement in survival were bladder, larynx, lip and brain cancers, and chronic lymphocytic leukaemia. Chemotherapy sessions accounted for 41% of these hospitalisations, followed by non-melanoma skin cancer (11%).
While the incidence of cancer is rising, the good news is that overall average mortality at the population level is falling and real improvements in survival are continuing.
The overall average is not necessarily indicative or representative of individual experience, where a diagnosis of cancer is anything but 'good news'. The observed fall in the overall cancer mortality rate can be mainly attributed to a combination of earlier detection (at a more treatable stage) and more effective treatments. Better survival rates for some cancers bring an increasing emphasis on living with, and after, a cancer diagnosis. Cancer contributed 16% of the total disease burden in Australasia (Australia and New Zealand), based on findings from the Global Burden of Disease Study 2010. The majority of health system expenditure on cancer in 2008–09 was on hospital-admitted cancer services (79%), followed by prescription pharmaceuticals (12%) and out-of-hospital services (9%).
That is, people diagnosed with cancer had a 66% chance of surviving at least 5 years compared with their counterparts in the general population.
The trend data presented here reflect the breadth (from first to most recent year) of available national data: 1982–2010 for incidence, 1968–2011 for mortality and 1982–1986 to 2006–2010 for survival. This increase reflects annual rises in the incidence of some of the most commonly diagnosed cancers such as prostate cancer, breast cancer and melanoma of the skin, as well as some rarer cancers such as liver and testicular cancers. This fall reflects substantial improvements in survival, thought to include substantial real gains in survival—that is, delaying death, and not only earlier diagnosis extending the measured time between diagnosis and death. This trend was observed for most, but not all, cancer types: survival from bladder, larynx and lip cancers fell, although the change was only significant for bladder cancer. Lung cancer incidence and mortality among males has declined steadily since the 1980s, which is attributed to the steadily declining rate in daily tobacco smoking: from 58% in 1964 to 16% in 2010.
There have been continuous falls in stomach cancer incidence between 1982 and 2010, and stomach cancer mortality between 1968 and 2011—2% and 3% per year, respectively. The AIHW and the Victorian Cytology Service recently conducted a study to evaluate the effectiveness of the HPV vaccine against cervical abnormalities among school-aged women (Gertig et al. BreastScreen Australia was introduced in 1991, the National Cervical Screening Program (NCSP) also started in 1991, and the National Bowel Cancer Screening Program (NBCSP) was introduced in 2006. Since it was introduced, BreastScreen Australia has had a major impact in moderating an increasing incidence trend and in contributing to falling mortality in breast cancer. The introduction of the NCSP resulted in a rapid decline (from an already decreasing trend) in cervical cancer incidence from 1991 to 2002, followed by a more stable trend to 2010 and a steady decline in cervical cancer mortality from 1991 to 2004, followed by a stable trend to 2010 (Figure 4.5B). It is likely, based on the continuation of current projected trends in incidence and mortality, that this population will continue to slowly rise over time, with an accompanying rise in the economic and social burden of cancer. It is more than simply not dying from cancer, and focuses on living with, and after, a cancer diagnosis (Jackson et al. While it is not possible with current available data to examine the incidence and prevalence of cancer as a comorbid condition, it is possible to use mortality data to analyse the proportion of Australians who have both cancer and other conditions recorded as causes of death. However, this type of analysis excludes those deaths where cancer was an associated cause of death, that is, any cause other than the underlying cause. Cancer was recorded as an associated cause in an additional 6,299 deaths, where the most common underlying causes were chronic ischaemic heart disease, acute myocardial infarction or other chronic obstructive pulmonary disease. Of these, 35% had only 1 cause recorded (the underlying cause), followed by 23% with 2 causes, 19% with 3 causes and 12% each with 4 and 5 or more causes.
All tips, guides and recommendations are followed at your own risk and should be followed up with your own research. Ita€™s urgent that we take swift action to effectively treat and prevent this serious disease."a€?Now is the time to take action. Glucose enters your red blood cells and links up (or glycates) with molecules of hemoglobin.
Drug company Abbott announced that its new ARCHITECT Clinical Chemistry Hemoglobin A1c (HbA1c) test – which can aid physicians in diagnosing and monitoring diabetes and identifying people at risk for the disease – has received 510(k) clearance from (FDA). Carefully following any medication orders and instructions is vital to your plan's success. Some say the prevalence is as high as 50 to 55% or 1 in 2 people, compared to the US norm of 1 in 5.
But when you consider all the ways that Diabetes can affect one’s health, their suspicion makes sense. In the US and Puerto Rico, some 44,000 people with Diabetes began treatment for end-stage kidney disease (aka renal disease) that year. In the second and third trimester, excessively large babies can result and pose a risk to mother and child.
We took these Elders generous fresh boxes of white meats (turkey and chicken), fresh produce, fresh fruit, and whole-grain products in the hopes that they would like some of these foods and add them to their diets. So is getting the amount of exercise needed to manage their weight; often they are too weak to do anything but sit in a chair. Arthritis also may directly relate to physical inactivity, which can lead to obesity and other chronic conditions. Physical inactivity is more common in adults who have both arthritis and heart disease compared with people who only have one or neither condition.
Physical inactivity is most common in adults who have both arthritis and diabetes compared with people who only have one or neither condition. Prevalence of doctor-diagnosed arthritis and arthritis-attributable activity limitation-United States, 2010-2012.
National diabetes fact sheet: general information and national estimates on diabetes in the United States, 2005. Normal beta-cell functionThe main role of beta-cell is to synthesize and secrete insulin in order to maintain circulating glucose levels within physiological range. Sites of pretranslational regulation by glucose of glucose-induced insulin release in pancreatic islets.
Indigenous and subnational breakdowns are key priorities for the current Australian Burden of Disease study. With changing lifestyles and ageing population, chronic diseases have become increasingly common and now cause most of the burden of ill health. There is great potential for integrating prevention and care, and treating selected chronic diseases together, to keep people healthy for as long as possible. They are a leading cause of disability, and have major impacts on health and welfare services (AIHW 2010). Once present, chronic diseases often persist throughout life, although they are not always the cause of death. The relative contribution of these causes to total deaths has also changed—for CHD the relative contribution fell from 33% in 1980 to 15% in 2011, and for cerebrovascular disease from 15% to 8%.
When a chronic disease is the underlying cause of death, other chronic diseases, such as cancers of unknown primary site, hypertensive diseases, and coronary heart disease, are common associated causes of death. A recent international study found that in Australia and New Zealand, chronic diseases together caused 85% of the total burden of disease, a similar figure to chronic diseases accounting for 90% of the burden due to deaths alone (IHME 2013). Two-thirds of the gap in death rates between Aboriginal and Torres Strait Islander and non-Indigenous people is contributed by chronic disease (AHMAC 2012).
People living in these same areas of disadvantage were 1.7 times as likely to report having 4 or more risk factors (AIHW 2012b). This proportion increases with age, so that among people aged 65 or older, 8% had 4 or more of these chronic diseases.
Others, such as coronary heart disease or cerebrovascular disease, are uncommon before adulthood, although the processes leading to their occurrence begin earlier in life. Adult risk factors for chronic disease also have their own histories; what people do or do not eat in adulthood, for example, is often established much earlier in life. For example, in-utero biological effects, combined with poor nutrition early in life, may affect how particular forms of fat are tolerated later in life. Seventy per cent of all cardiovascular disease mortality in Australia has been attributed to the combined effects of high blood pressure, high cholesterol and physical inactivity (Begg et al.
Females with 5 or more risk factors are 3 times as likely to have had a stroke, and two and a half times as likely to have depression as females with 2 or fewer risk factors (AIHW 2012b). Daily smoking is also more commonly reported by people with low levels of physical activity. These changes, together with timely and better medical treatments, are important in improving chronic disease health outcomes. Assessing the risk of cardiovascular disease on the basis of the combined effect of multiple risk factors (absolute cardiovascular disease risk) can lead to better management of modifiable risk factors through lifestyle changes and pharmacological therapy (National Vascular Disease Prevention Alliance 2012).
Despite a decline in cancer deaths and an increase in survival over time, cancer is still the second-most common cause of death in Australia—after cardiovascular diseases.
This was driven by rises in the incidence of prostate, breast and bowel cancers, due largely to improved detection and diagnosis of these cancers. The fall in mortality rates was driven by falls in lung, prostate and bowel cancer death rates among males, and falls in breast and bowel cancer death rates among females. The 26-year prevalence was highest for breast cancer (151,152 women), melanoma of the skin (136,016), prostate cancer (129,978 men) and bowel cancer (105,144).


The number of cancer-related deaths is attributable to changes in risk factor exposure and the ageing of the population. Carcinoma is a cancer that begins in the skin or in tissues that line or cover internal organs. Expenditure on national population screening programs was just over $332 million in 2008–09. In contrast, the incidence of some cancers, including lung, bladder and cervical, fell significantly in that same period.
There has been a gain in the overall trend in more recent years, with mortality falling by an average of 1.0% per year from 1991 to 2011. In contrast, for females, lung cancer incidence and mortality among females continue to rise. Similarly, the NCSP has had a major impact in enhancing decreasing trends for cervical cancer incidence and mortality (Figure 4.5).
It also means a challenge for the health system in responding to these changes, particularly with an ageing population.
Many cancer support organisations and groups recognise the importance and growing size of this population, and provide support to carers, siblings and friends of people with cancer (Cancer Council Victoria 2011).
In total, 49,520 deaths in that year (34%) included cancer as a cause of death (either underlying or associated).
The proportion of deaths reported as being caused by 3 or more causes rose from 32% in 1997 to 42% in 2011 (Figure 4.7). If these numbers continue to rise, 1 in 5 people could have diabetes by the year 2025, and it could be 1 in 3 people by the year 2050. Think about this and you will understand the dilemma of all who dwell with Diabetes, especially our American Indian friends to the North and South who need your help. Although there exist several triggers of insulin secretion like nutrients (amino acids such as leucine, glutamine in combination with leucine, nonesterified fatty acid), hormones, neurotransmitters and drugs (sulfonylurea, glinides), glucose represents the main physiological insulin secretagogue [1].According to the most widely accepted hypothesis, insulin secretion is a multistep process initiated with glucose transport into beta-cell through specific transporters (GLUT1 and GLUT2 in particular) and phosphorylation by glucokinase, which directs metabolic flux through glycolysis, producing pyruvate as the terminal product of the pathway [2]. Notably, mental health-related issues are not a major cause of death, but they do cause significant ill health and disability in the Australian population (see Chapter 4 'Mental health in Australia'). Indigenous people report diabetes at more than 3 times the rate of other Australians, and rates of treatment for end-stage kidney disease are more than 7 times as great. Arthritis and high blood pressure are 2 conditions that commonly occur together among adults. Today's children, who are subject to increased behavioural risks at earlier ages through the consumption of energy-dense foods and poor diet, increased screen time and reduced physical activity, will live longer with risk factors such as obesity (Amschler 2002; Swinburn et al. Observing risk factors and chronic disease development in populations from an early age can provide valuable lessons for future disease management. Early social disadvantage may interact with affluence in later life to increase coronary heart disease risk. Similarly, around half of people aged 65–74 had to cope with 5 or more chronic diseases, increasing to 70% of those aged 85 and over (AIHW 2012a). Identifying populations most at risk and monitoring and evaluating preventive interventions are also important (AIHW 2011b). These strategies all involve better delivery and coordination across the health-care continuum, from health promotion and prevention, to early detection where appropriate, and to primary, secondary and tertiary care. Cancer has a significant impact on individuals, families and the health-care system and has had a prominent policy focus for decades. Sarcoma is a cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue. There has been a moderation in the overall trend in more recent years, with incidence rising by an average of 0.5% per year from 2001 to 2010. This study demonstrated that the population-based HPV vaccination program in Australia is preventing cervical pre-cancer lesions in young women, with a fall in cervical abnormalities after the program was implemented in 2007 (Gertig et al.
Cancer survivors often face emotional, physical and financial challenges as a result of the detection, diagnosis and treatment of cancer.
This shift away from the acute care setting is also apparent in palliative care, with a South Australian study reporting that 70% of respondents would prefer to die at home than elsewhere, if faced with a terminal illness such as cancer (Foreman et al. We simply cana€™t sustain this trajectory a€“ the implications are far too great a€“ for our families, our healthcare system, our workforce, our nation."a€?We know today that adopting a healthier lifestyle is the most effective way to prevent type 2 diabetes and improve health for people already diagnosed with diabetes. By measuring the percentage of A1C in the blood, you get an overview of your average blood glucose control for the past few months. Of course, Type II diabetes can be controlled with proper diet, weight management, and exercise, and sometimes insulin or other medications.
Pyruvate then enters the mitochondria and is decarboxylated to acetyl-CoA, which enters the tricarboxylic acid cycle.
Despite the falls in death rates and relative contributions to total deaths, the number of people dying from chronic diseases is still large because of Australia's growing and ageing population (see Chapter 6 'Ageing and the health system'). Indigenous people were almost twice as likely as non-Indigenous people to report having asthma. Cholesterol, blood pressure and overweight measures at young ages often persist into adulthood, and can predict the later occurrence of coronary heart disease.
GPs and their teams can perform a key role in screening and prevention, and coordinating services (RACGP 2012). Leukaemia is a cancer that starts in blood-forming tissue, such as the bone marrow, and causes large numbers of abnormal blood cells to be produced and enter the blood. The moderated trend after the 1980s is consistent with increased awareness of skin cancer and improved sun protective behaviours as a result of extensive skin cancer prevention programs dating back to the 1970s (AIHW 2012a). Further improvements in incidence and mortality are expected as a result of the continued decreasing trend in daily smoking. The tricarboxylic acid cycle proper begins with a condensation of acetyl-CoA and oxaloacetate, to form citrate, a reaction catalysed by citrate synthase.
Accordingly, rates of hospitalisation and death are higher among Indigenous people (see Chapter 7 'How healthy are Indigenous Australians?'). Having multiple chronic conditions is associated with worse health outcomes, more complex disease management and increased health costs (AIHW 2012b).
Based on current knowledge, the future impact of these behavioural risks on individuals, populations and the health system will be significant.
Smoking habits acquired in adolescence or early adulthood greatly increase the risk for cardiovascular diseases and COPD in adulthood and old age—along with cancers and many other chronic diseases.
Such an approach can strengthen and transform health-care systems, resulting in more effective, efficient, and timely care (Standing Council on Health 2013). The effect of the vaccine is expected to increase over time as women vaccinated at age 12–13 become eligible to be screened in the cervical screening program and enter the age ranges where cancer incidence is more common.
The age of quitting smoking is also important and a major influence in reducing later COPD, coronary heart disease, and other chronic disease risk.
Central nervous system cancers are cancers that begin in the tissues of the brain and spinal cord. This is an area where gains may also follow for other cancers with a similar viral aetiology (see Glossary) to cervical cancer. How do we become resistant to insulin and what causes our beta cells to fail?Insulin resistance can develop as a result of fat cells releasing more pro-inflammatory chemicals such as IL-6, and fewer anti-inflammatory chemicals such as adiponectin. NAD-linked isocitrate dehydrogenase then oxidatively decarboxylates isocitrate to form ?-ketoglutarate. The ?-ketoglutarate is oxidised to succinyl-CoA in a reaction catalysed by ?-ketoglutarate dehydrogenase. Succinyl-CoA synthase then catalyses the conversion of succinyl-CoA to succinate, with the concomitant phosphorylation of GDP to GTP.
That is not what some of my textbooks say, which claim that type 2 diabetes has a stronger genetic component than type 1 diabetes. Unfortunately their authors have been lazy and taken the fact that type 2 diabetes runs in families as evidence of a genetic link.
Prevention efforts nationwide are crucial to combat serious health risks.Individuals can learn more about diabetes and prediabetes by talking to a healthcare provider about the risk to them and their families. Fumarase catalyses the conversion of fumarate to malate and after that malate dehydrogenase catalyses the ?nal step of the tricarboxylic acid cycle, oxidising malate to oxaloacetate and producing NADH.Three pathways enable the recycling of the tricarboxylic acid cycle intermediates into and out of mitochondrion, allowing a continuous production of intracellular messengers [3-5].
It is all to do with the fact that people in the same family follow a similar dietary pattern, and often a similar exercise pattern as well. Learn more about diabetes and CDCa€™s evidence-based and cost-effective interventions through our National Diabetes Prevention Program. In fact type 1 diabetes has a much stronger genetic component with a few genes on chromosome 6 being responsible for much of the susceptability. May 12, 2016 Why Vitamin D Is More Important than You Think April 28, 2016 3 Practical Steps to Fight Stress & Soothe Anxiety April 5, 2016 Recent CommentsUKadmin on GLA vs.
Malate exits the mitochondria to the cytoplasm where it is subsequently oxidised to pyruvate concomitant with the production of NADPH by cytosolic malic enzyme. In type 2 diabetes a large number of genes are associated with risk and none particularly strongly.What happens in the diabeticThere are some tissues in our body that let glucose in without insulin. Citrate then exits the mitochondrion to the cytoplasm where it is converted back to oxaloacetate and acetyl-CoA by ATP-citrate lyase. Fat and muscle cells contain GLUT-4 transporters, which don't allow much glucose in without insulin being present.
Oxaloacetate is converted by cytosolic malate dehydrogenase to malate before being converted to pyruvate by malic enzyme.
The brain on the other hand has a lot of GLUT-3 transporters, which allow appreciable amounts of glucose in without insulin being present.Tissues which let in glucose without insulin are found in the eye, kidneys, peripheral nervous system as well as the liver, ovaries and seminal vesicles. The unfortunate result for these cells is that they can accumulate too much glucose over time. About Your Health KeysYour Health Keys is a go-to source for the latest news, tools and tips to educate and inspire healthy living. The NADPH oxidase complex in the plasma membrane is also activated through protein kinase C, which is activated by fatty acid derived signalling molecules. However, those cells in the eyes, kidneys and in our peripheral circulation accumulate sorbitol, which causes swelling of the cells due to osmotic pressure.
These events result in an enhanced ratio of ATP to ADP in the cytoplasm, which determines the closure of the ATP-sensitive K+ channels, depolarization of the plasma membrane, influx of extracellular Ca2+ and activation of exocytosis which takes place in several stages including recruitment, docking, priming, and fusion of insulin granules to the beta-cell plasma membrane [1,6,7].
Two independent studies, using diazoxide for maintaining the ATP-sensitive K+ channels in the open state or mice in which the ATP-sensitive K+ channels were disrupted, indicated that glucose –stimulated insulin secretion can also occur independently of ATP-sensitive K+ channels activity [8].Under physiological conditions, there is a hyperbolic relation between insulin secretion and insulin sensitivity. Most of these complications result from raised levels of glucose in cells which do not rely on insulin to obtain it. Classically, glucose-stimulated insulin secretion is characterized by a first phase, which ends within a few minutes, and prevents or decreases glucose concentration and a more prolonged second phase in which insulin is released proportionally to the plasma glucose [9].In addition, it has been demonstrated that the release of insulin is oscillatory, with relatively stable rapid pulses occurring at every 8-10 minutes which are superimposed on low-frequency oscillations [10]. In particular some cells lining capillaries and nerves in the kidneys, eyes and limbs are vulnerable.
Place of beta-cell dysfunction in natural history of type 2 diabetesT2DM is a progressive condition caused by genetic and environmental factors that induce tissue insulin resistance and beta-cell dysfunction.
Based on the United Kingdom Prospective Diabetes Study (UKPDS) and on the Belfast Diabetes Study, it is estimated that at diagnosis of T2DM, beta-cell function is already reduced by 50-60% and that this reduction of beta-cell function seems to start with 10-12 years before the appearance of hyperglycemia [11,12].
Several lines of evidence indicated that there is no hyperglycemia without beta-cell dysfunction [13,14]. In most subjects with obesity-induced insulin resistance developing increased insulin secretion, insulin gene expression and beta-cell mass, these compensatory mechanisms can succeed to maintain glucose homeostasis and avoidance of diabetes mellitus [13-15]. As a result they leak proteins which ultimately result in constriction of the blood vessels supplying the kidney. In the phase which precedes overt diabetes the decline of beta-cell function is slow but constant (2% per year) [19]. Since the brain uses sugar as its main energy source it goes to plan B which is creating ketones, which can provide energy also. After the development of overt hyperglycemia there appears a significant acceleration (18% per year) in beta-cell failure, and the beta-cell function deteriorates regardless of the therapeutic regimen [11,19,20].
Too many ketones acidify our blood and cause excess urination, thirst, vomiting and tummy pain. Ultimately severe dehydration, swelling of the brain and coma can occur, which is why hospitalisation is often needed. This is a serious complication of type 1 diabetes.
Consequent deterioration in metabolic equilibrium with increasing levels of glucose and free fatty acids, enhance and accelerate beta-cell dysfunction, lead to beta-cell apoptosis that does not seems to be adequately compensated by regenerative process and subsequent decrease of beta-cell mass.4. However, it is uncommon with type 2 as some insulin is normally available.Curing diabetes naturallyExercising more and consuming foods that do not raise blood sugar levels is the key to reversing diabetes.
Potential mechanism and modulators of beta-cell failureThe main focus of the present chapter is on potential beta-cell failure mechanisms in T2DM.The initial alterations in beta-cell function are likely to reflect intrinsic defects, whereas the accelerated beta-cell dysfunction which mainly occurs after the development of overt hyperglycemia is the consequence of glucolipotoxicity [21]. While it becomes harder to regain full health the longer you have had diabetes, when first diagnosed, the vast majority of people have the potential to completely cure themselves of the condition.The correct dietThe modern western diet is the main cause of diabetes. This reflects a genetic predisposition for beta-cell defect, whereas the subsequent beta-cell failure may be a consequence of concomitant environmental conditions. Genetic factorsSeveral genes associated with increased risk of developing T2DM have been identified in genome-wide association studies [22]. For instance on one of my GI lists I have a baked potato with a GI of 111, greater than pure glucose while peanuts are listed with a GI of just 7, which implies that foods containing the East Asian sauce, satay would be very low GI.
Genetic variation in this gene obviously affects the beta-cell excitability and insulin secretion [23].HHEX encodes a transcription factor necessary for the organogenesis of the ventral pancreas [49] and two SNPs (rs1111875, rs7923837) in HHEX were found to be associated with reduced insulin secretion [24-26]. SLC30A8 encodes the protein zinc transporter 8, which provide zinc for maturation, storage and exocytosis of the insulin granules [50]. So in other words the GI is not an absolute value, but just a guideline. Sometimes it is more realistic to consider the glycaemic load or GL of a food, which takes account of the amount of a food you eat.
Variants in this gene show to be associated with reduced glucose-stimulated insulin secretion [25,27] and alterations in proinsulin to insulin conversion [42].
Obviously one Cornflake (GI=93) is not going to raise blood sugar as much as a whole can of baked beans (GI=40), but a small bowl of them probably will.Foods that are normally low GI can be eaten as the main part of a diet for someone with diabetes. These include meat, fish, eggs, dairy as well as nuts, seeds, most vegetables and some fruits. The one vegetable that has a high GI is the potato (this includes the sweet potato), and the fruits with a high GI include ripe bananas, dates and raisins. GlucolipotoxicityGrowing evidence indicated that long-term elevated plasma levels of glucose and fatty acids contribute to beta-cell function decline, a phenomenon known as glucolipotoxicity. Generally speaking fruits from warm climates have a higher GI than those from more temperate climates. Glucolipotoxicity differs from beta-cell exhaustion, which is a reversible phenomenon characterized by depletion of insulin granules due to prolonged exposure to secretagogues. Chronic exposure of beta-cells to hyperglycemia can also induce beta-cells apoptosis by increasing proapoptotic genes expression (Bad, Bid, Bik) while antiapoptotic gene expression Bcl-2 remains unaffected [54].There is a strong relationship between glucotoxicity and lipotoxicity.
For instance if you exercise soon after consuming the food then some of the blood sugar it creates will be taken up by your muscle cells.
Thus, hyperglycemia increases malonyl-CoA levels, leading to the inhibition of carnitine palmitoyl transferase-1 and subsequently to decreased oxidation of fatty acids and lipotoxicity [52].
If you combine it with other foods of much lower GI or eat a small portion of it you will also find your blood sugar does not rise as far.Timing foodsIn general if you exercise then you will reduce your blood sugar level.
Increased fatty acids in the pancreas leads to intrapancreatic accumulation of triglycerides [55]. A 30 minute exercise stint before food will allow you to get away with a higher overall glycaemic load.
Lim E et al showed that the intrapancreatic fat is associated with beta-cell dysfunction and that sustained negative energy balance induces restoration of beta-cellular function [56].Elevated levels of glucose and saturated fatty acids in beta cells, stimulates AMP-activated protein kinase, which contributes to increased expression of sterolregulatory-element-binding-protein-1c (SREBP1c), leading to increased lipogenesis [57].
Equally if you do some light exercise soon after a large meal you can lower the peak which your blood sugar will reach.In general it is best to leave some time between any meal and completely sedentary activity such as bed or watching the TV. Kids get it about right when they automatically rush about after a meal, often to the frustration of their bloated parents.
Activation of the isoform of protein kinase C (PKC?) by free fatty acids which has been suggested as a possible candidate signaling molecule underlying the decrease in insulin secretion [60].Impaired insulin gene exepression by down-regulation of PDX-1 and MafA insulin gene promoter activity [61]. A bit of housework, gardening or short walk are often quite effective at making a real dent in your blood sugar readings.Treating diabetes with drugsIt really is best to avoid the need for drugs. PDX-1 is affected in its ability to translocate to the nucleus, whereas MafA is affected at the level of its expression [61].
I would always advise making concerted efforts to control blood sugar levels with increases in exercise and changes to the diet. Free fatty acid impairs insulin gene expression only in the presence of hyperglycemia [62]. Many people find they can come off drugs completely when they do this properly.For those who cannot control their blood sugar levels without drugs then it is sensible to take them. Palmitate affects both insulin gene expression and insulin secretion, unlike oleate which affects only insulin secretion [63]. The cumulative effect over time of high blood sugar levels is extremely damaging, and this is why so many diabetics suffer from amputations, blindness, heart attacks and strokes.Blood sugar lowering agentsThe main one is perhaps Metformin which lowers the amount of sugar your liver produces. Thiazilienediones such as Rosiglitazone increase insulin sensitivity of the tissues and glucosidase inhibitors such as Acarbose reduce absorption of glucose from the gut. All these drugs will be more or less effective in different people depending on how their diabetes is affecting them. Measuring blood sugar levelsDiabetes is diagnosed using criteria that are arbitrary. Endoplasmic reticulum stressThe endoplasmic reticulum is responsible for the protein synthesis, being involved in protein translation, folding and assessing quality before protein secretion. There are several ways that are used to measure blood sugar problems:Fasted blood sugar level - FBGThis measures blood sugar levels after not eating anything for at least 8 hours.
Accumulation of unfolded and misfolded protein in the endoplasmic reticulum lumen may impose endoplasmic reticulum stress [79,80]. However, this value will vary depending on factors such as stress, recent exercise and illness. Inflammatory cytokines such as IL-1? and IFN-?, can also cause endoplasmic reticulum stress [72].Endoplasmic reticulum stress induced beta-cell activation of an adaptive system named unfolded protein response by which it attenuates protein translation, increases protein folding and promotes misfolded protein degradation [81,82]. Thus, it prevents additional protein misfolding and further accumulation of unfolded protein; increase the folding capacity of the endoplasmic reticulum to deal with misfolded proteins via the induction of endoplasmic reticulum chaperones.
Secondly their muscles get used to using fat as a fuel place of glucose and so more glucose is left in the blood. Mitochondrial dysfunction and ROS productionBeta cell mitochondria play a key role in the insulin secretion process, not only by providing energy in the form of ATP to support insulin secretion, but also by synthesising metabolites that can act as factors that couple glucose sensing to insulin granule exocytosis [3].Mitochondrial dysfunction and abnormal morphology occur before the onset of hyperglycemia and play an important role in beta-cell failure [89]. If you come into this category the measure below could be more useful to you.Long term blood sugar controlTo assess this we measure the amount of glycosylated haemoglobin - HbA1c, in your red blood cells. In diabetic state, the proteins from the mitochondrial inner membrane are decreased, and also may exist transcriptional changes of the mitochondrial proteins [89].
Haemoglobin - Hb, is the protein found in red blood cells that is responsible for carrying oxygen to your tissues. Mitochondrial dysfunction, induced by glucolipotoxicity, plays a pivotal role in beta-cell failure and leads to increased ROS production as a result of metabolic stress. In good health somewhere between 3-5% of our haemoglobin is in the HbA1c form.Red blood cells live for an average of 120 days.
Levels of antioxidant enzymes in beta cells are very low (catalase and glutathione peroxide levels were much lower than those of superoxide dismutase), making beta cells be vulnerable to oxidative stress [92].Low concentrations of ROS contribute to increased glucose-stimulated insulin secretion, but only in the presence of glucose-induced elevations in ATP [93]. There are a number of factors that can skew the measurement:People with healthy low blood sugar have longer lived red blood cells that may survive for an average of 150 days. In this case a high end reading for HbA1c does not imply bad blood sugar control.Diabetics with high blood sugar levels have red blood cells that live shorter lives than average, typically around 90days.
All these effects are reversible in time after transient increase ROS.Chronic and significant elevation of ROS, resulted from an imbalance between ROS production and scavenging by endogenous antioxidants, may lead to beta-cell failure [95,96].
Persistent oxidative stress mediates beta-cell failure through several different mechanisms, including:Decreased insulin secretion. It may be a better measure than HbA1c, and gives an indication of blood sugar levels over the previous 2-3 weeks(5).Glucose challenge or OGTTThe oral glucose tolerance test - OGTT is a measure of our response to consuming 75g of glucose in one hit. Beta-cells lipid accumulation via SREBP1c [108].The antioxidant effect varies depending on the type of exposure of beta cells to ROS. It is unrealistic as most people never consume such a large and purified amount of glucose.
Thus, under beta-cells exposure to low concentrations of ROS, antioxidants lower the insulin secretion [109,110]. Instead, under the glucolipotoxicity, antioxidants increase the insulin secretion and reduce beta cell apoptosis [108].9.
Additionally, beta-cells dysfunction and apoptosis may also be triggered by pro-inflammatory signals from other organs, such as adipose tissue [111,112].
For most people achieving the low GI meal involves limiting the amount of starchy carbohydrates they eat. Chronic exposure of beta-cell to inflammatory cytokines, like Il-1?, IFN-? or TNF-?, can cause endoplasmic reticulum stress and the unfolded protein response activation in beta-cells, and also beta-cells apoptosis [72,115]. Because, as indicated by Donath et al, the apoptotic beta-cells can provoke, in turn, an immune response, a vicious cycle may develop [115].
Another cytokine involved in beta-cells dysfunction is the PANcreatic DERived factor (PANDER). There have not been revealed significant effects of adiponectin on basal or glucose-stimulated insulin secretion [112].Leptin is another adipocytokine that may interfere with beta-cell function and survival. In studies on animal model, leptin has been shown to inhibit insulin secretion via activation of ATP-regulated potassium channels and reduction in cellular cAMP level [116], inhibit insulin biosynthesis by activating suppressor of cytokine signalling 3 (SOCS3) [119], suppress acetylcholine-induced insulin secretion [116] and induce the expression of inflammatory genes [120]. Studies performed on human islets indicated that chronic exposure to leptin stimulates the release of IL-1? and inhibits UCP2 expression, leading to beta-cell dysfunction and apoptosis [111].
Other adipocytokines including TNF-?, IL-6, resistin, visfatin may also modulate beta-cell function and survival, although it is unclear whether the amount released into the circulation is sufficient to affect beta-cells [111].10.
Islet amyloid polypeptideHuman islet amyloid polypeptide (amylin) is expressed almost exclusively in beta-cells and is costored and coreleased with insulin in response to beta-cells secretagogues.
Glucolipotoxicity causes increased insulin requirement and those lead to increased production of both insulin and amylin. High concentrations of amyloid are toxic to beta-cells and have been implicated in beta-cell dysfunction and apoptosis [121,122].The effect of Islet amyloid polypeptide on beta-cell function is not fully elucidated. Studies in vivo have shown that the islet amyloid polypeptide inhibits the first and second phase of glucose-stimulated insulin secretion, but this occurs only at concentrations of islet amyloid polypeptide above physiological range [77].
Beta-cell failure — Implication for treatmentUnderstanding the causes for beta-cell failure is of capital importance to develop new and more effective therapeutic strategies.Taking into consideration the existence of early beta-cell dysfunction and the significant reduction of beta-cell mass in the natural history of T2DM as well as the progressive character of these pathophysiological modifications, insulin therapy could be an important option for obtaining and maintaining an optimal glycemic control. Several lines of evidence indicated that metformin could improve beta-cell function and survival.
Incubation of T2DM islets with metformin was associated with increased insulin content, insulin mRNA expression and glucose responsiveness, and also with reduced cell apoptosis by normalization of caspase 3 and caspase 8 activities [103]. It has been shown that metformin, and also the PPAR gamma agonists can protect beta-cell from deleterious effects of glucolipotoxicity [126,127].Other therapeutic options for beta-cell protection, such as incretins are actually under debate.



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