Diabetes mellitus type 2 and cardiovascular disease journal,type 2 diabetes extreme tiredness weakness,jan hoet kritiek - Plans Download


Science, Technology and Medicine open access publisher.Publish, read and share novel research. Age is an Important Risk Factor For Type 2 Diabetes Mellitus and Cardiovascular DiseasesKetut Suastika1, Pande Dwipayana1, Made Siswadi Semadi1 and RA Tuty Kuswardhani2[1] Division of Endocrinology and Metabolism, Internal Medicine, Faculty of Medicine, Udayana University, Sanglah Hospital, Denpasar, Indonesia[2] Division of Geriatrics; Department of Internal Medicine, Faculty of Medicine, Udayana University, Sanglah Hospital, Denpasar, Indonesia1. Akbaraly TN, Kivimaki M, Ancelin ML, Barberger-Gateau P, Mura T, Tzourio C, Touchon J, Ritchie K, Berr C. Hayashi T, Kawashima S, Itoh H, Yamada N, Sone H, Watanabe H, Hattori Y, Ohrui T, Yokote K, Nomura H, Umegaki H, Iguchi A; Japan CDM Group. Holvoet P, Kritchevsky SB, Tracy RP, Mertens A, Rubin SM, Butler J, Goodpaster B, Harris TB. Kirwan JP, Khrisnan RK, Weaver JA, Del Aguila LF, Evans WJ.Human aging is associated with altered TNF-a production during hyperglycemia and hyperinsulinemia.
Minamino T, Orimo M, Shimizu I, Kunieda T, Yokoyama M, Ito T, Nojima A, Nabetani A, Oike Y, Matsubara H, Ishikawa F, Komuro I.
Poehlman ET, Berke EM, MI Joseph JR, Gardner AW, Ades PA, Katzan-Rook SR, Goran MI.Influence of aerobic capacity, body composition, and thyroid hormone on age-related decline in resting metabolic rate. Type 2 diabetes mellitus has become an epidemic, and virtually no physician is without patients who have the disease. Diabetes mellitus has reached epidemic proportions and affects more than 170 million individuals worldwide. The medical and socioeconomic burden of the disease is caused by the associated complications,7-9 which impose enormous strains on health-care systems. Although lifestyle and overeating seem to be the triggering pathogenic factors, genetic elements are also involved in the pathogenesis of type 2 diabetes. Since dizygotic twins share the environment (both intrauterine and extrauterine) but only 50% of their genes, concordance rates in monozygotic twins in excess of those in dizygotic twins have been used to distinguish genetic from non-genetic contributions. Nevertheless, concordance rates in monozygotic twins might produce an underestimate of genetic effects, because the monochorionic intrauterine nutrition of monozygotic twins has been shown to result in growth retardation compared with dizygotic twins.32 And low birthweight itself is associated with increased risk of type 2 diabetes later in life.
To understand the cellular and molecular mechanisms responsible for type 2 diabetes it is necessary to conceptualise the framework within which glycaemia is controlled. In people with normal glucose tolerance (NGT) a quasi-hyperbolic relation exists between ß-cell function and insulin sensitivity. However, not only deviation from but also progression along the hyperbola affects glycaemia. Insulin resistance is said to be present when the biological effects of insulin are less than expected for both glucose disposal in skeletal muscle and suppression of endogenous glucose production primarily in the liver.38 In the fasting state, however, muscle accounts for only a small proportion of glucose disposal (less than 20%) whereas endogenous glucose production is responsible for all the glucose entering the plasma.
Insulin secretion from the pancreas normally reduces glucose output by the liver, enhances glucose uptake by skeletal muscle, and suppresses fatty acid release from fat tissue.
Insulin resistance is strongly associated with obesity and physical inactivity, and several mechanisms mediating this interaction have been identified. To understand the contribution of insulin resistance in a particular tissue to whole body glucose homoeostasis, conditional knockouts of the insulin receptor have been created using the Cre-lox system. In states of insulin resistance, one or more of the following molecular mechanisms to block insulin signalling are likely to be involved.
Insulin signalling involves binding of insulin to its receptor followed by a cascade of intracellular events, depicted as activation pathways. A close connection between insulin resistance and classic inflammatory signalling pathways has also recently been identified.
In ß cells, oxidative glucose metabolism will always lead to production of reactive oxygen species, normally detoxified by catalase and superoxide dismutase.
Islet amyloid consists of deposits of islet amyloid polypeptide, also known as amylin, which is co-secreted with insulin at a more than tenfold lower rate. It is possible that early in the disease, increased demands of insulin secretion lead to islet amyloid polypeptide aggregates, especially in the presence of raised concentrations of NEFA. Although there is little doubt as to the importance of genetic factors in type 2 diabetes (table 2), it should be borne in mind that this disease is very heterogeneous. The candidate gene approach examines specific genes with a plausible role in the disease process. The candidate gene approach in attempts to identify a causative factor among the obvious biological candidates for insulin resistance has been largely disappointing (table 4).
Among the many candidate genes for insulin secretory dysfunction, those encoding SUR1 and KIR6·2 have been most extensively studied. Genes involved in embryonic ß-cell development, such as components of the insulin-like growth factor pathways, have also been studied.
Several findings of positive associations of genomic regions with type 2 diabetes have been replicated in one or more studies (1q21-24, 1q31-q42, 9q21, 10q23, 11p15, 11q13-14, 12q12, 19q13, and 20q11-q13 ).114 Generally, such findings are followed by positional cloning of the causative gene, which to date has not been successful for most regions. A peculiar possibility is the relation of diabetes to imprinted genes--ie, genes for which expression varies depending on the sex of the transmitting parent.
In making therapeutic choices (figure 7) in the management of type 2 diabetes, the major goal of protecting patients from the long-term complications of the disease must be considered. Drugs that enhance insulin sensitivity are primarily those of the thiazolidinedione class, which not only reduce glycaemia, but also enhance vascular function and ameliorate the dyslipidaemia and inflammatory milieu of type 2 diabetes.131 Thiazolidinediones primarily activate PPARgamma receptors in adipose tissue and alter adipose metabolism and distribution.
Unlike metformin, the thiazolidinediones can be used in patients with reduced renal function, and they are better tolerated without significant gastrointestinal side-effects. Metformin is a highly effective antihyperglycaemic drug that works independently of the pancreas, sparing insulin. As inadequate ß-cell insulin secretion is fundamental to the development of hyperglycaemia in diabetes, insulin secretion enhancers also play an important role in control of blood glucose.
The mode of action of sulfonylurea derivatives implies that they also act at low concentrations of plasma glucose, which explains the potential of (occasionally severe) hypoglycaemia. The recently introduced class of meglitinides consists of nateglinide, which binds to the same site of sulphonylurea receptor 1 as do the sulfonylurea derivatives, and repaglinide, which binds to a nearby site of the receptor, both leading to insulin release.
Replacing circulating concentrations of insulin is essential to support the clinical effects of metformin and the thiazolidinediones, which are ineffective without adequate insulin availability, and may also have important beneficial effects in reducing inflammatory processes, especially in the vasculature.142 Thus, it is essential to initiate insulin injections when required to achieve glycaemic targets in type 2 diabetes, possibly in combination with oral insulin sensitisers. As specific drug targets are identified through improved understanding of the molecular pathogenesis of diabetes, novel therapeutics will become available in the future. The results of the HOPE study,147 in which use of ramipril was associated with a markedly lower risk of myocardial infarction, stroke, and death, favour use of the ACE inhibitor in diabetic patients with one additional risk factor, even if they do not have hypertension. The benefit of lipid-lowering drugs has now been firmly established, since the Scandinavian Simvastatin Survival Study showed a reduction in total mortality of 43%. Fibric acid derivatives might benefit diabetic patients because they raise concentrations of HDL cholesterol and reduce triglyceride levels.
Whether therapy should be given for other risk factors such as hyperhomocysteinaemia (treated with folic acid), and whether antioxidants are of use, is still unclear because of the absence of studies with hard endpoints in patients with type 2 diabetes. The goal of ultimately reducing the population burden of diabetes by early treatment and prevention is clearly of pivotal importance. A more complete understanding of the molecular mechanisms of diabetes will enable the identification of individuals at highest risk, which could lead to novel pharmacological concepts, risk stratification, and development of more targeted preventive measures. Diabetes is what diabetes in dogs red eyes hartford connecticut causes low blood sugar most often Type 2 diabetes is also called type 2 diabetes mellitus and adult-onset diabetes.
Zostrix Diabetic Foot Pain Relieving Cream with Capsaicin provides effective strong pain relief for those that suffer from the discomfort sugar level range in human body la new orleans associated with diabetic foot pain. Gestational diabetes can increase your risk of high blood pressure while you’re pregnant.
Diabetes is the primary reason for adult blindness, end-stage renal disease (ESRD), gangrene and amputations.
Though, Diabetes mellitus is not completely curable but, it is controllable to a great extent. New improved Insulin and its therapy, (external and implantable insulin pumps) have advanced well to manage elevated blood sugars without any allergic reactions. New improved blood glucose monitor (new device for self blood glucose monitoring), and hemoglobin A1c laboratory test to measure blood glucose control during previous 3 months. Exercise is an effective treatment for type 2 diabetes mellitus, resulting in stabilization of plasma glucose in the acute phase and improvements in body composition, insulin resistance and glycosylated haemoglobin with chronic exercise training. If you have answered yes to 3 or more of these, then you may be suffering from weight gain or you may have already reached obesity! Insulin resistance occurs when the normal amount of insulin secreted by the pancreas is not able to unlock the door to cells. No one knows for sure.A  Some scientists think a defect in specific genes may cause insulin resistance and type II diabetes. Research indicatesA  that low fat diets may aggravate the effect of insulin resistance on blood lipids. The good news is I have found a way to help you or a loved one overcome Insulin resistance. This is not a quick fix weight loss programme; this is a medically based weight loss program, which has already helped many of my patients. Frequency of metabolic syndrome (MS), impaired fasting glycemia (IFG), and diabetes mellitus (DM) in the younger-aged and elderly.
IntroductionA field study by World Health Organization (WHO), World Bank and Harvard University in 1990 found a changing pattern of diseases caused by unhealthy lifestyle changes that may eventually lead to metabolic syndrome, type 2 diabetes mellitus, coronary arterial diseases, depression, and traffic accidents (Kinsella and Phillips, 2005). Low HDL cholesterol is associated with the risk of stroke in elderly diabetic individuals: changes in the risk for atherosclerotic diseases at various ages. The metabolic syndrome, circulating oxidized LDL, and risk of myocardial infarction in well-functioning elderly people in the health, aging, and body composition cohort. High liporotein (a) level promotes both coronary atherosclerosis and myocardial infarction: a path analysis using a large number of autosy cases. Whereas insulin insensitivity is an early phenomenon partly related to obesity, pancreas ß-cell function declines gradually over time already before the onset of clinical hyperglycaemia. The incremental costs of patients with type 2 diabetes arise not only when the diagnosis is established but at least 8 years earlier.10 The devastating complications of diabetes mellitus are mostly macrovascular and microvascular diseases as a consequence of accelerated atherogenesis.
Insulin is the key hormone for regulation of blood glucose and, generally, normoglycaemia is maintained by the balanced interplay between insulin action and insulin secretion.
When insulin action decreases (as with increasing obesity) the system usually compensates by increasing ß-cell function. Endogenous glucose production is accelerated in patients with type 2 diabetes or impaired fasting glucose.39,40 Because this increase occurs in the presence of hyperinsulinaemia, at least in the early and intermediate disease stages, hepatic insulin resistance is the driving force of hyperglycaemia of type 2 diabetes (figure 3). The various factors shown that contribute to the pathogenesis of type 2 diabetes affect both insulin secretion and insulin action. A number of circulating hormones, cytokines, and metabolic fuels, such as non-esterified (free) fatty acids (NEFA) originate in the adipocyte and modulate insulin action.
Among the five conditional insulin receptor knockouts shown in table 3, only liver47 and ß-cell specific knockouts50 became glucose intolerant whereas, unexpectedly, knockout models specific for muscle46 and fat cells48 did not.
Negative modulation of insulin action can be mediated via various pathways leading to insulin resistance: various inhibitory triggers affect their respective signal modulators (partly via transcription factors), which lead through deactivating pathways (tyrosine phosphatases, serine kinases, lipid phosphatases and degradation pathways) to inhibitory actions on insulin signalling (activation pathways).
Basal insulin concentrations may be raised to roughly double the usual value, especially in obese hyperglycaemic patients, but this finding is presumably due to increased plasma glucose. Further degradation leads to formation of pyruvate, which is then taken up in the mitochondria in which further metabolism leads to ATP formation. Generally, in both non-diabetic and diabetic obese patients, NEFA concentrations are raised as a result of enhanced adipocyte lipolysis.
The physiological role of islet amyloid polypeptide is unclear, and diverse roles such as inhibition of insulin action, inhibition of insulin secretion, and inhibition of glucagon secretion have been proposed. The finding that first-degree relatives of patients with type 2 diabetes have decreased islet amyloid polypeptide (and insulin) responses to intravenous glucose, however, challenges this speculation.96 Also, amyloid is not observed in middle-aged insulin-resistant individuals.
For this purpose the statistical association of a given allele and a phenotype (eg, type 2 diabetes, or insulin resistance) is tested in unrelated individuals. The two genes--ABCC8 and KCNJ11, respectively--are adjacent to one another on chromosome 11.
Genetic variation near or in the P2-promoter of the MODY-1 gene HNF4A gene (chromosome 20q) has been proposed to relate to common type 2 diabetes,128 but this finding requires independent confirmation. The class III allele of the variable number tandem repeat near the insulin gene (chromosome 11p15) might relate to type 2 diabetes.129 The class III allele is associated with decreased amounts of insulin mRNA. Because insulin resistance plays a fundamental role in the pathogenesis of type 2 diabetes and especially its adverse cardiovascular outcomes, interventions should initially be aimed towards improvement in tissue insulin sensitivity. The redistribution of tissue triglyceride from visceral stores reduces levels of circulating NEFA apparently by sequestration in a less lipolytic subcutaneous compartment.132 Thiazolidinediones also reduce circulating concentrations of pro-inflammatory cytokines that promote insulin resistance (eg, TNFalpha and interleukin 6) and at the same time increase concentrations of adiponectin, which has insulin-sensitising and anti-inflammatory properties.
A major adverse effect associated with clinical use of the thiazolidinediones is weight gain, which seems to be coupled to the effects of the drugs on adipose cell differentiation and triglyceride storage. It decreases hepatic glucose output and has been shown to have a beneficial effect on cardiovascular outcomes.136-138 Metformin has less robust effects on insulin resistance, inflammatory markers, and vascular function compared with the thiazolidinediones, but its benefit in abrogating some of the weight gain commonly observed with insulin-sensitisers and insulin secretion enhancers adds important value to this drug.
Sulfonylurea derivatives act by closing pancreatic cell potassium channels, which leads to enhanced insulin secretion. These agents cannot further stimulate insulin release in patients on maximal doses of sulfonylurea derivatives. However, combined use of insulin and thiazolidinediones seems to infer an increased risk of oedema and cardiac failure.
This incretin hormone has potent glucose-dependent insulinotropic properties, trophic effects on ß cells, and inhibitory effects on intestinal motility, all of which reduce plasma glucose. Conversely, increasing adiponectin secretion or administration of an adiponectin receptor agonist would probably enhance glucose metabolism in skeletal muscle and liver and also confer beneficial effects in the endothelium. The benefit of antihypertensive therapy is larger in diabetic than in non-diabetic hypertensive patients. They can decrease endothelial cell activation possibly because of their capacity for binding PPARalpha.
A number of studies have shown that diabetes can be delayed or prevented in individuals at high risk undergoing an intensive diet and exercise programme, and intervention with medications including metformin, acarbose or thiazolidinediones has also shown to be effective (table 5). A long-term goal is to develop drugs that restore normoglycaemia by targeting specific pathogenic defects.
Those with diabetes are at high risk for a number of complicationsComplication of diabetes and treatmentsThanks to the efforts of two Canadian physicians, Frederick Banting and Charles Finest, insulin was discovered and this drastically changed the lives of millions diabetics, specially those suffering from insulin-dependent diabetes mellitus (IDDM), the far more severe form of the illness. There are two main types of dabetes mellitus and they are Blood Glucose Level Chart Diabetes Illinois Rockford type 1 and type 2. Before I mention diabetes in early pregnancy symptoms oxnard california a couple of methods through which you can prevent or even treat diabetes I want to make sure you know the difference between the two types of Compared to type 1 diabetes Blood Glucose Level Chart Diabetes Illinois Rockford type 2 is also called non-insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes. It is a metabolic disorder in which human body does not produce or properly uses insulin, a hormone that is required to convert sugar, starches, and other food into energy.
Human body has to maintain the blood glucose level at a very narrow range, which is done with hormone insulin. When breakdown of glucose is stopped completely, body uses fat and protein for producing the energy.
Overweight, lack of exercise, family history and stress increase the likelihood of diabetes.
However, the most appropriate exercise prescription for type 2 diabetes has not yet been established, resulting from insufficient evidence to determine the optimum type, intensity, duration or frequency of exercise training.
When too much glucose is present in the body, the pancreas increases the amount of insulin being produced.A  High insulin as well as high glucose may contribute to multiple symptoms. Therefore, for individuals who are insulin resistant, a diet low in saturated fat (less than 10 percent of total calories) and more moderate in total fat content (40% of total calories) may be beneficial. I have been practising as a homeopath for the past 6 years and I myself have picked up weight and tried exercising, dieting and even medication, but nothing was able to give me a lasting result. The program first starts by getting your mental and physical body in shape, yes the mind is extremely important for weight loss.


The study also predicted that cerebrovascular diseases would become the most prevalent disease, whereas human HIV infection would sharply increase in the year 2020 (Kinsella and Phillips, 2005). Several mechanisms have been proposed, including increased non-esterified fatty acids, inflammatory cytokines, adipokines, and mitochondrial dysfunction for insulin resistance, and glucotoxicity, lipotoxicity, and amyloid formation for ß-cell dysfunction. Importantly, the normal pancreatic ßcell can adapt to changes in insulin action--ie, a decrease in insulin action is accompanied by upregulation of insulin secretion (and vice versa).
An increased mass of stored triglyceride, especially in visceral or deep subcutaneous adipose depots, leads to large adipocytes that are themselves resistant to the ability of insulin to suppress lipolysis.
These findings clearly support a central role of hepatic insulin resistance in the pathogenesis of type 2 diabetes, and suggest that an adequate insulin signal in the pancreatic ß cell is needed to maintain its function. Adiponectin has an ameliorating function on glucose metabolism apart from insulin signalling.
Similarly, after a meal, concentrations of insulin in plasma can appear higher than normal, because of substantially raised plasma glucose. ATP is necessary for the delivery of energy needed for the release of insulin, but it is also involved in the cell membrane depolarisation. Fatty acids lead to enhanced insulin secretion in acute studies, but after 24 h they actually inhibit insulin secretion.
It has been suggested that small aggregates are cytotoxic,94 possibly related to radical production. Thus, the role of amyloid deposits (a post-mortem finding) in pancreatic islets in the pathophysiology of type 2 diabetes remains unclear. In general, two methods are used for studying genetic factors involved in a specific disease: the so-called candidate gene approach and the genome-wide scan approach.
The genome-wide scan or linkage approach is not based on assumptions but locates genes through their genomic position and is based on the rationale that family members sharing a specific phenotype will also share chromosomal regions surrounding the gene involved. This often involves lifestyle intervention, with modest exercise and weight loss, which clearly reduces the risk of progression of impaired glucose tolerance to overt diabetes12,13 and can improve many of the cardiovascular risk parameters of the metabolic syndrome.
Fluid retention is also linked to the PPARgamma-agonist activity of the thiazolidinediones, leading to peripheral oedema and a mild haemodilution in some patients. The results of the UK Prospective Diabetes Study8 showed a clear risk reduction for the occurrence of microvascular complications by the use of sulfonylurea derivatives, while the risk reduction of macrovascular disease was around 16%. However, because circulating glucagon-like peptide 1 is immediately inactivated by dipeptidyl peptidase IV, it is therapeutically impractical.
Recent evidence for amelioration of insulin resistance by salicylates by favourable interference with the inflammatory kinase cascade in insulin signalling might lead to entirely novel therapeutic approaches. The interesting observation that improvement in one or more major pathogenic factors offsets the progression of impaired glucose tolerance to diabetes underscores the contribution of each of these factors to the development of the disease, including insulin sensitivity, ß-cell function, and actual glucose excursions.
One example would be to advance the thiazolidinedione concept to design compounds that could restore defects in individuals with a defective PPARgamma regulatory system.
But in the obese leptin levels are often found to be high due to resistance to its action at the cell level. Prompt and aggressive treatment of diabetic foot ulcers can often prevent exacerbation of the problem and how often do you get ultrasounds when you have gestational diabetes boston massachusetts eliminate the potential for amputation.
In general Type I diabetes has a highly significant overall association with Blood Types A and AB and this is especially strong in males versus females.
Ringkasan CPG Diabetes Mellitus 2009 oleh Dr Siti Gestational Diabetes Mellitus oleh SN Nik Rozilan Medication Error and ADR Reporting by Mr Adnan I A complete medical history including a family medical history will be taken. Whether you have type 1 or type II diabetes or gestational diabetes, the goals of achieving control of blood glucose levels are similar: to keep blood (Lupus, Muscle Weakness, Fatigue) (Complete Article).
Symptoms like polydipsia, polyuria, polyphagia, and excessive weightloss can be observed in a diabetic due to this mechanism.
When blood sugar level is constantly high it leads to kidney failure, cardiovascular problems and neuropathy. A number of conditions are associated with insulin and glucose imbalances and regulation problems. This recommendation is different from the low-fat, high-carbohydrate diet that many health organizations recommend to help prevent heart disease.A  Specifically, they recommend decreasing fat intake to less than 30 percent of calories. The second phase teaches you how to correctly introduce foods that will assist your body to lose the excess weight and the third phase is a life long phase that helps you maintain your new weight. The lifestyle-related and degenerative diseases are significant problems in the old aged population group.The number of elderly population has increased worldwide, and recently it has been increasing sharply in the developing countries.
Elliott, Metabolic alterations in middle-aged and elderly obese patients with type 2 diabetes. Thus, even with (theoretically) unlimited ß-cell reserve, insulin resistance paves the way for hyperglycaemia and type 2 diabetes.
Insulin resistance pathways affect the action of insulin in each of the major target tissues, leading to increased circulating fatty acids and the hyperglycaemia of diabetes. Additionally, reactive oxygen species are known to enhance NFkappaB activity, which potentially induces ß-cell apoptosis. Fortunately, congestive heart failure is quite rare with use of thiazolidinediones, but remains a serious concern that requires caution in selection of patients to receive these agents.135 The ability of thiazolidinediones to ameliorate risk of atherosclerotic events is being assessed in several large outcomes studies.
Thus, careful attention needs to be applied to determine appropriate public interventions for the varied populations of the world.
There are many likely reasons for low engagement in exercise; one possible contributory factor may be a tendency for expert bodies to prioritize the roles of diet and medication over exercise in their treatment guidelines. These include chronic stress, polycystic ovarian syndrome (PCOS),coronary artery disease, high blood pressure, metabolic syndrome, and diabetes.
Even people with diabetes who take oral medication or require insulin injections to control their blood glucose levels can have higher than normal blood insulin levels due to insulin resistance.
The projection of the number of elderly population in Indonesia by the year 2010 is 23,992.
Suastika, Age and homocystein were risk factor for peripheral arterial disease in elderly with type 2 diabetes mellitus. Management includes not only diet and exercise, but also combinations of anti-hyperglycaemic drug treatment with lipid-lowering, antihypertensive, and anti platelet therapy. Thus, ß-cell dysfunction is a critical component in the pathogenesis of type 2 diabetes.
In turn, the raised concentrations of glucose and fatty acids in the bloodstream will feed back to worsen both insulin secretion and insulin resistance.
The closure of the potassium channels will alter the membrane potential and open calcium channels, which triggers the release of preformed insulin-containing granules (figure 5). However, long-chain acyl coenzyme A itself can also diminish the insulin secretory process by opening ß-cell potassium channels (figure 6).
Combined management with both sulfonylurea derivatives and antihypertensives improves the risk reduction even more.
Lifestyle modification has been difficult to maintain over a long term, and has costs associated with regular visits to various health-care professionals and lifestyle coaches.
Antisense inhibition of PTP1B, a tyrosine phosphatase, currently undergoing phase II trials, could become the treatment of choice for patients with a genetic variant in PTP1B.156 Generally, with an optimised risk-benefit ratio, patients who respond to treatment may also benefit from specific drugs in a preventive approach. Each IDDM and non-insulin dependent diabetes mellitus (NIDDM) have brief and lengthy term risks. Published treatment guidelines vary in their approach to exercise training, but most agencies suggest that people with type 2 diabetes engage in 150A min of moderate to vigorous aerobic exercise per week. National diabetes fact sheet: general information and national estimates on diabetes in the United States. The Indonesian Central Bureau for Statistics (Badan Pusat Statistik) has reported that Indonesia is the world’s fourth in the number of elderly population after China, India, and USA (Komala et al., 2005). A second mechanism might be increased expression of uncoupling protein-2, which would lead to reduced ATP formation and, hence, decreased insulin secretion.
Until that day, diet and exercise remain the pillars of prevention and treatment of type 2 diabetes.
Untreated, the illness have an effect on and harm blood vessels in the brain, the head, the eyes, the legs and the kidneys.1 acute complication of IDDM is ketoacidosis which typically occurs when the diabetic fails to get insulin injections or is under anxiety from illness or injury. This prescription is similar to the established guidelines for cardiovascular health in the general population. US Bureau of Census predicted that from 1990 to 2020, the Indonesian elderly population would increase to 41.4%. A third mechanism might involve apoptosis of ß cells, possibly via fatty acid or triglyceride-induced ceramide synthesis or generation of nitric oxide. Further clinical trials comparing these and newer medications that may affect diabetes pathogenesis (such as glucagon-like peptide 1 analogues) are needed to balance safety and efficacy with the costs of these different agents in various regions.
The implementation and sensible use of the available pharmacological agents, including insulin, and the management of other cardiovascular risk factors, remain the practical challenge to the clinician. As blood sugar levels rise, chemical compounds referred to as ketones form, producing the blood far more acidic.This outcomes in increased urination and thirst, weakness and drowsiness, vomiting, diarrhea, and a sweet smelling breath as acetone is getting expelled from the lungs. Future possibilities in this area include investigation of the physiological effects and practical benefits of exercise training of different intensities in type 2 diabetes, and the use of individualized prescription to maximize the health benefits of training.
The predicted increased number of elderly was ascribed to the success of health promotion and improvement of social and economic status (Kinsella and Taeuber, 1993). Women who have had gestational diabetes are very likely to develop type 2 diabetes later in life. Exercise prescription for patients with type 2 diabetes and pre-diabetes: a position statement from exercise and sport science Australia.
Metabolic disorders including type 2 diabetes mellitus (T2DM) and cardiovascular diseases are closely related with the aging process. Nemeth, Histochemical and enzymatic comparison of the gastrocnemius muscle of young and elderly men and women.J. Ketoacidosis is most most likely in the undiagnosed diabetic or in a individual whose diabetes is not properly-controlled,” mentioned Dr. GESTATIONAL DIABETES - Gestational diabetes only affects about 4% of all expecting mothers. Central obesity and insulin resistance as the initial preconditions and its consequences related to metabolic diseases and cardiovascular diseases are frequently found among the elderly. Donath, Aging correlates with decreased ?-cell proliferative capacity and enhanced sensitivity to apoptosis.
Decline in lean body mass and increase in body fat, particularly visceral adiposity that often accompanies aging, may contribute to the development of insulin resistance.
Bolli, Demonstration of a critical role for free fatty acids in mediating counter regulatory stimulation of gluconeogenesis and suppression of glucoseutilization in humans. Larson, editor-in chief of the Mayo Clinic Family members Well being Book.“However, any diabetic is topic to ketoacidosis under such circumstances as accidental injury, infection, or loss of significant quantities of fluid by way of vomiting or diarrhea. To examine the prediction of gestational diabetes in obese women using routine clinical measures and measurement of biomarkers related to insulin resistance in the early second trimester. As for the mechanism of T2DM, it is known that aging induces a decrease of insulin sensitivity and alteration or insufficient compensation of beta cell functional mass in the face of increasing insulin resistance (Meneilly and Elliot, 1999).
Ducimetiere, The metabolic syndrome and the carotid artery structure in non-institutionalized elderly subjects.
Related to beta cell functions, aging correlates with a decrease of beta cell proliferation capacity and enhances sensitivity to apoptosis (Maedler et al., 2006). Young, Effect of age on energy expenditure and substrate oxidation during experimental overfeeding in healthy men. These incorporate hypertension, coronary artery illness, and atherosclerosis (the formation of fatty deposits in the arteries that minimize the flow of blood to crucial organs) all of which make a individual susceptible to stroke, heart attack, and gangrene of the feet.These are caused by the deterioration of nerves and significant blood vessels. It has recently been proposed that an age-associated decline in mitochondrial function contributes to insulin resistance in the elderly (Petersen et al., 2003). Lima, Age-related left ventricular remodeling and associated risk for cardiovascular outcomes.
Gerich, Effect of aging on glucose homeostasis: Accelerated deterioration of ?-cell function in individuals with impaired glucose tolerance. If the modest blood vessels are involved, blurred vision and other eye troubles could happen. The illness is a significant trigger of blindness in the globe even although there are a couple of diabetic patients who fully shed their sight.
Lamb, The ageing male heart: myocardial triglyceride content as independent predictor of diastolic function. It also produces decreased skin sensitivity that could lead to severe ulcerations in the limbs and ultimately bring about one more quite severe complication: gangrene leading to amputation,’ added the editors of World Well being, a publication of the World Well being Organization (WHO).
Age, mitochondrial dysfunction and inflammationMitochondria, a membrane-enclosed organelle found in most eukaryotic cells, generate most of the cell's supply of adenosine triphosphate (ATP), are used as a source of chemical energy, and are involved in a range of other processes such as signaling, cellular differentiation, cell death, as well as the control of the cell cycle and cell growth.
Mitochondria have been implicated in several human diseases, including mitochondrial disorders, aging process and cardiac dysfunction. And point of thinking is we have most critical aspects of life right now, with a enormous level risk of creating diabetes. Mitochondrial dysfunction is central to the theories of aging because age-related changes of mitochondria are likely to impair a host of cellular physiological functions in parallel and thus contribute to the development of all the common age-related diseases (Dai et al., 2012). Rising cellular oxidative stress due to any cause induces mtDNA and mitochondria damage and culminates in a mitochondria function crisis, cell death and aging. Diabetic retinopathy is the most frequent such dilemma, despite the fact that cataracts and glaucoma are somewhat far more most likely in the diabetic than in the non-diabetic” Larson revealed. Otherwise, aging itself causes abnormal mitochondrial morphology and cell death or apoptosis (Seo et al., 2010).
Hyperglycemia, hyperosmolar stateTypically referred to as HNS, the symptoms are related to DFA, but in a fully diverse source. Cost-sparing effect of twice-weekly targeted endurance training in type 2 diabetics: a one-year controlled randomized trial. How old age can be a major risk factor for CVD via mitochondrial dysfunction has been completely reviewed by Dai et al.
Training-induced improvement in lipid oxidation in type 2 diabetes mellitus is related to alterations in muscle mitochondrial activity: effect of endurance training in type 2 diabetes. The role of NF-?B in bridging the explanation of how aging is associated with inflammation and endothelial dysfunction is reviewed well by Csiszar et al. Otherwise, the organization is nonetheless dry and closed.HypoglycemiaRarely, but nonetheless at risk of hypoglycemia when blood sugar levels are really low.
In the case of diabetes, this could be due to the truth that when sufficient insulin or can not have the time appropriate. Another study has shown that depletion of cellular (GSH) during aging plays an important role in regulating the hepatic response to IL-1? (Rutkute et al., 2007). At rest, skeletal muscles of elderly people showed a lower number of macrophages, higher gene expression of several cytokines, and activation of stress signaling proteins, compared with skeletal muscles of young people (Peake et al., 2010).
Ten-year experience with an exercise-based outpatient life-style modification program in the treatment of diabetes mellitus. Human aging is associated with the development of insulin resistance, ?-cell dysfunction and glucose intolerance. The level of suppression of the TNF-? production was observed and found to be significantly correlated with insulin action. Reduced suppression of TNF-? production in the elderly may in part contribute to the decline in insulin sensitivity (Kirwan et al., 2001).
Effects of aerobic training, resistance training, or both on glycemic control in type 2 diabetes: a randomized trial. Age and lipid metabolismAging and age are often associated with lipid metabolism disorders.


Intravenous dextrose is the most frequent therapy in the hospital.Diabetic ketoacidosisThis complication named diabetic acute is normally constantly a medical emergency. Effects of aerobic and resistance training on hemoglobin A1c levels in patients with type 2 diabetes: a randomized controlled trial.
After the age of 20 years, low-density lipoprotein cholesterol (LDL-C) increases significantly in both men and women. LDL-C does not increase or is in a flat state between the age of 50-60 years (male) and 60-70 years (female) (Gobal and Mehta, 2010).
On the other hand, high–density lipoprotein cholesterol (HDL-C) levels decrease during puberty to young adulthood (in males).
Physical activity advice only or structured exercise training and association with HbA1c levels in type 2 diabetes: a systematic review and meta-analysis. Throughout their lives women have lower total cholesterol compared to men, but the levels will rise sharply after menopause and will be higher in the age >60 years as compared to men.
Even so, if this method is sustained over a lengthy period of ketenes in the blood lowers the phi here is a DFA. Concentrations of triglyceride (TG) increase sharply in males, reaching a peak at the age 40-50 years and decline gradually thereafter. If you create diabetic acute is normally quite dry and challenging, deep breath, as if exhausted. TG levels increase in women throughout their lives, especially in women taking estrogen replacement therapy (Gobal and Mehta, 2010). Effects of exercise on glycemic control and body mass in type 2 diabetes mellitus: a meta-analysis of controlled clinical trials.
With the increase of age the composition of body fat also increases, which especially accumulates in the abdomen triggering the incidence of central obesity. Even though men and women are conscious sufficient to slow a individual and as a result of lethargy could create later in a coma. TG composition in the muscle and liver are higher in older age compared with younger age groups (Cree et al., 2004). Increased body fat composition is associated with reduced fat oxidation both at rest and in activity (Nagy et al., 1996).
Effects of different modes of exercise training on glucose control and risk factors for complications in type 2 diabetic patients: a meta-analysis. Aging (age) affects the release of fatty acids (FFA),from fat tissue (adipose), and the capacity of peripheral tissues such as muscles, to oxidize fat. These are some of the changes in lipid metabolism influenced by age and aging, which decreases lipolysis response and capacity of fat oxidation.Lipolysis is modulated by various hormones such as catecholamines, glucagon, adrenocorticotropic hormone, growth hormone, prostaglandin, and thyroid hormone (Toth and Tchernof, 2000). Even so, if therapy is delayed or incomplete, the probability of death increases drastically.As you can see the acute complications of diabetes is one thing you want to prevent at all expenses. Decreased ability of catecholamines to stimulate lipolysis in the elderly is caused by decreased fat tissue response to adrenergic stimulation (Dillon et al., 1984). This response involves reduced role of protein kinase A, G-protein complex adenylil cyclase, or the stages in the cyclic AMP signaling cascade (Toth and Tchernof, 2000).
Effects of insulin on plasma FFA was different between in the elderly compared with in younger subjects. Additive effects of glycaemia and blood pressure exposure on risk of complications in type 2 diabetes: a prospective observational study (UKPDS 75).
Insulin infusions showed that plasma FFA, turnover and oxidation, and total lipid oxidation were higher significantly in the elderly than in the younger group (Bonadonna et al., 1994). Aging is also associated with decreased sensitivity to antilipolysis effects of insulin (Toth and Tchernof, 2000). The impact of training modalities on the clinical benefits of exercise intervention in patients with cardiovascular disease risk or type 2 diabetes mellitus.
In principle, the capacity of metabolically active tissues such as the muscles to oxidize fat represents a combination of the tissue mass and oxidative capacity of the tissue. Fat free mass decreases with age (Poehlman et al., 1992) and in resting condition fat oxidation tends to be influenced by the size of fat free mass itself.
Changes in lipid metabolism in the aging process are associated with dysfunction of endothelial cells pseudocapillarization of the liver sinusoid.
Diet and exercise among adults with type 2 diabetes: findings from the third national health and nutrition examination survey (NHANES III).
This change causes decreased endocytosis, increased leukocyte adhesion, decreased hepatic perfusion and will potentially reduce the passage of chylomicron remnants into hepatocytes (Denke and Grundy, 1990). After activity or after meal, fat oxidation rate is more influenced by the oxidative capacity of muscle tissue. Disposal of non-oxidative free fatty acids into the liver will increase the formation of triglyceride-rich very low-density lipoprotein (VLDL) that plays a role in the formation of atherogenic dyslipidemia. Increased levels of TG and decrease HDL-C are features of atherogenic dyslipidemia in people with central obesity, hypertension and insulin resistance (Linblad et al, 2001).
Educational disparities in health behaviors among patients with diabetes: the Translating Research Into Action for Diabetes (TRIAD) Study. Lower HDL cholesterol is an important risk factor for not only ischemic heart disease but also for cerebrovascular disease, especially in diabetic elderly individuals (Hayashi et al., 2009).
Health care and patient-reported outcomes: results of the cross-national Diabetes Attitudes, Wishes and Needs (DAWN) study. Age, insulin resistance and metabolic syndrome Metabolic syndrome is a group of metabolic abnormalities of which central obesity and insulin resistance are believed to be the primary backgrounds. The diagnostic criteria for metabolic syndrome have been proposed by several organizations and associations, all of which are based on five parameters i.e. The pathogenesis of how central obesity causes insulin resistance and metabolic syndrome has been explained in many publications. Decreased insulin sensitivity, reduced muscle mass, and increased body fat mass, especially visceral fat that accompanies aging contribute to insulin resistance in the elderly. Are health care professionals advising patients with diabetes or at risk for developing diabetes to exercise more? Aging process is also associated with reduced compensatory beta cell mass function of the pancreas and to insulin resistance (Maneilly and Elliott, 1999) as well as with decreased mitochondrial function that contributes to insulin resistance (Petersen et al., 2003).
Insulin resistance as risk factor for cardiovascular disease (CVD) is associated with increase of acute phase protein response and inflammatory markers. The association of metabolic syndrome and increased frequency of carotid plaque and thickening of the carotid artery intima media in elderly subjects (aged 65-85 years) was noted in a study by Empana et al. Metabolic syndrome in the elderly was associated with two-times increase of CRP levels (3.1 vs.
A comparison of views of individuals with type 2 diabetes mellitus and diabetes educators about barriers to diet and exercise. Sports activities >2 hours per week would be effective in lowering the risk of metabolic syndrome. Age and type 2 diabetes mellitus Similar to metabolic syndrome, the prevalence of impaired fasting glycemia (IFG) and T2DM increase with rising age. In the United States, the estimated percentage of people aged 20 years or older having diagnosed or undiagnosed diabetes in 2005-2008 was increasing with age.
Similar feature was also observed n England, where the prevalence of diabetes was increasing with age.
There was a tendency of increasing frequency of IFG and T2DM with increasing age (Table 2).
American Association of Clinical Endocrinologists medical guidelines for clinical practice for the management of diabetes mellitus.
Global Guideline for type 2 diabetes: recommendations for standard, comprehensive, and minimal care. Hypertension, overt proteinuria, IFG and high total cholesterol were independent risk factors for new onset diabetes (Peng et al., 2006).
The main factors are that aging induces decrease insulin sensitivity and alteration or insufficient compensation of beta cell functional in the face of increasing insulin resistance (Chang and Halter, 2003). Canadian Diabetes Association 2008 clinical practice guidelines for the prevention and management of diabetes in Canada.
Decrease in beta cell proliferation capacity and enhanced sensitivity to apoptosis are the states related with aging (Maedler et al., 2006). But aging per se has no effect on insulin sensitivity independent of change in body composition.
Decline in lean body mass and the increase in body fat particularly visceral adipocytes (“central obesity”) that accompanies aging may contribute to insulin resistance.
It has recently been proposed that an age-associated decline in mitochondrial function contributes to insulin resistance in elderly.
Mitochondrial oxidative and phosphorylation function was reduced about 40% in association with increased intramyocellular and intrahepatocellular lipid content and decreased insulin-stimulated glucose uptake (Petersen et al., 2003).
The pathophysiological basis of sarcopenia (loss of muscle mass with age) has a relationship with oxidative stress, reduced neuronal stimulation, subclinical inflammatory and insulin resistant state. Those conditions contribute to the development of glucose intolerance and type 2 diabetes (Khamseh et al., 2011).
They also proposed that adipose tissue p53 tumor suppressor mediated the lipid abnormalities and cardiovascular morbidity associated with obesity. The study found that excessive calorie intake caused accumulation of oxidative stress in the adipose tissue of mice with type 2 diabetes–like disease and promoted senescence-like changes, such as increased activity of senescence-associated ?-galactosidase, increased expression of p53 and increased production of proinflammatory cytokines. Inhibition of p53 activity in adipose tissue decreased the expression of proinflammatory cytokines and improved insulin resistance. Age and cardiovascular diseases Cardiovascular disease remains to be the most important cause of death in all countries over the world.
Although certain reports from some developed countries indicate the incidence tends to decrease, from many countries there are reports mentioning that its incidence tends to increase.
Cardiovascular disease is a complex disease; too many risk factors are involved in its pathogenesis. In general, risk factors for CVD can be divided into two main groups, namely traditional and non-traditional risk factors. Age itself may be an independent risk factor or may have other risk factors related to aging or exposure to risk factors during their lifetime.
In the United States, CVD was the leading cause of death for persons 65 years of age and over in 2007, which accounted for 28% of deaths in this age group (National Center for Health Statistics, 2011). Adherence to exercise prescriptions: effects of prescribing moderate versus higher levels of intensity and frequency. Age in the group with CHD (old myocardial infarction and myocardial ischemia) was significantly higher than those without CHD (65.0 vs. This increase includes luminal enlargement with wall thickening and a reduction of elastic properties at the level of large elastic arteries. Long standing arterial pulsation in the central artery has a direct effect on the structural matrix proteins, collagen and elastin in the arterial wall, disrupting muscular attachments and causing elastin fibers to fatigue and fracture.
Endurance exercise intensity determination in the rehabilitation of coronary artery disease patients: a critical re-appraisal of current evidence.
Increased vascular calcification and endothelial dysfunction is also characteristic of arterial aging. These changes lead to increased pulse wave velocity, especially along central elastic arteries, and increase in systolic blood pressure and pulse pressure (Lee and Oh, 2010). Aging cardiovascular tissues are exemplified by pathological alterations including hypertrophy, altered left ventricular (LV) diastolic function, and diminished LV systolic reverse capacity, increased arterial stiffness, and impaired endothelial function. Continuous low- to moderate-intensity exercise training is as effective as moderate- to high-intensity exercise training at lowering blood HbA(1c) in obese type 2 diabetes patients. This pattern of ventricular remodeling confers significant cardiovascular risk, particularly when present earlier in life. Substrate oxidation during exercise: type 2 diabetes is associated with a decrease in lipid oxidation and an earlier shift towards carbohydrate utilization. Peripheral artery disease (PAD), a marker of systemic atherosclerosis, is frequently related with age. Substrate source utilisation in long-term diagnosed type 2 diabetes patients at rest, and during exercise and subsequent recovery. A study by Kuswardhani and Suastika (2010) on elderly patients who visited the Geriatric Outpatient Clinic, Sanglah Hospital showed that diabetic patients with PAD had higher age (70.7 vs. Metabolic training: new paradigms of exercise training for metabolic diseases with exercise calorimetry targeting individuals. By multivariate analysis (logistic regression), it was found that only age played a role in PAD event.
ConclusionThe number of elderly population has increased worldwide, and recently it has been increasing sharply in the developing countries.
Prolong survival in the elderly creates an impact on the appearance of metabolic diseases and CVD.
Physiological adaptations to low-volume, high-intensity interval training in health and disease.
Acute high-intensity interval exercise reduces the postprandial glucose response and prevalence of hyperglycaemia in patients with type 2 diabetes.
Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes.
High-intensity interval running is perceived to be more enjoyable than moderate-intensity continuous exercise: implications for exercise adherence. Effects of preferred-exercise prescription compared to usual exercise prescription on outcomes for people with non-specific low back pain: a randomized controlled trial [ACTRN12608000524392]. Individual assessment of intensity-level for exercise training in patients with coronary artery disease is necessary. Efficacy of exercise interventions in modulating cancer-related fatigue among adult cancer survivors: a meta-analysis. Individualized 12-week exercise training programs enhance aerobic capacity of cancer survivors. Exercise tolerance testing in a cardiac rehabilitation setting: an exploratory study of its safety and practicality for exercise prescription and outcome data collection. Influences of age and exercise on glucose metabolism: implications for management of older diabetics.
Exercise considerations in coronary artery disease, peripheral vascular disease, and diabetes mellitus. Exercise training improves glycemic control in long-standing insulin-treated type 2 diabetic patients. Brisk walking compared with an individualised medical fitness programme for patients with type 2 diabetes: a randomised controlled trial.
Prescription of physical activity is not sufficient to change sedentary behavior and improve glycemic control in type 2 diabetes patients. The prevalence and cost of diabetes in metropolitan France: what trends between 1998 and 2000? Effects of a personal trainer and financial incentives on exercise adherence in overweight women in a behavioral weight loss program. Financial motivation undermines maintenance in an intensive diet and activity intervention.



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