Statistics for type 2 diabetes in ireland zip,diabetic neuropathy cures,type 2 diabetes under 30 06,genomics type 2 diabetes and obesity n engl j med genet - New On 2016

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.
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. 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 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.
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.
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. 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.
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 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. 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. 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. This makes it impossible for someone with diabetes to depend on another person for the around the clock control and still remain active. 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. 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.
Ita€™s urgent that we take swift action to effectively treat and prevent this serious disease."a€?Now is the time to take action. 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. 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]. 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. 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. By measuring the percentage of A1C in the blood, you get an overview of your average blood glucose control for the past few months. There are many professionals who provide diabetes education and guide the person through the self-management of diabetes.
Pyruvate then enters the mitochondria and is decarboxylated to acetyl-CoA, which enters the tricarboxylic acid cycle.
Of course, Type II diabetes can be controlled with proper diet, weight management, and exercise, and sometimes insulin or other medications. 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. The tricarboxylic acid cycle proper begins with a condensation of acetyl-CoA and oxaloacetate, to form citrate, a reaction catalysed by citrate synthase. 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. 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]. 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. Learn more about diabetes and CDCa€™s evidence-based and cost-effective interventions through our National Diabetes Prevention Program.


Malate exits the mitochondria to the cytoplasm where it is subsequently oxidised to pyruvate concomitant with the production of NADPH by cytosolic malic enzyme. Citrate then exits the mitochondrion to the cytoplasm where it is converted back to oxaloacetate and acetyl-CoA by ATP-citrate lyase. Oxaloacetate is converted by cytosolic malate dehydrogenase to malate before being converted to pyruvate by malic enzyme.
The NADPH oxidase complex in the plasma membrane is also activated through protein kinase C, which is activated by fatty acid derived signalling molecules. 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. 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]. 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]. In the phase which precedes overt diabetes the decline of beta-cell function is slow but constant (2% per year) [19]. 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]. 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. 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]. 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]. 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].
Variants in this gene show to be associated with reduced glucose-stimulated insulin secretion [25,27] and alterations in proinsulin to insulin conversion [42]. 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.
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. 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].
Increased fatty acids in the pancreas leads to intrapancreatic accumulation of triglycerides [55]. 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]. 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]. PDX-1 is affected in its ability to translocate to the nucleus, whereas MafA is affected at the level of its expression [61]. Free fatty acid impairs insulin gene expression only in the presence of hyperglycemia [62].
Palmitate affects both insulin gene expression and insulin secretion, unlike oleate which affects only insulin secretion [63].
Endoplasmic reticulum stressThe endoplasmic reticulum is responsible for the protein synthesis, being involved in protein translation, folding and assessing quality before protein secretion. Accumulation of unfolded and misfolded protein in the endoplasmic reticulum lumen may impose endoplasmic reticulum stress [79,80]. 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.
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]. In diabetic state, the proteins from the mitochondrial inner membrane are decreased, and also may exist transcriptional changes of the mitochondrial proteins [89].
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.
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]. 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.
Beta-cells lipid accumulation via SREBP1c [108].The antioxidant effect varies depending on the type of exposure of beta cells to ROS.
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]. 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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