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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. The second stage diabetes, also known as the Type 2 diabetes is a severe medical condition that develops with the increase in the level of glucose in the body. It usually affects people who are over 40 years of age, but nowadays even younger people are observed to experience the Type-2 diabetes. It is very essential to maintain a healthy weight throughout your life to control the levels of blood sugar.
In addition to several main causes, there are other causes that can lead to second stage diabetes.
During the past several years, the incidence of type 2 diabetes has increased.  Type 2 diabetes is an outcome of a combination of lifestyle and genetic elements. Diabetes poses the risk for many conditions mainly because due to poorly controlled blood sugar levels. With time, the high glucose levels in the blood can cause damage to the nerves and small blood vessels affecting the eyes, kidney and heart. Other long term complications can appear as poor circulation (leading to amputation), diabetic retinopathy, kidney failure and ketoacidosis. Hyperglycemia is an outcome arising out of an excessively raised blood sugar level in diabetes. Due to the buildup of sugar in blood, there can be increased urination causing the kidneys to lose glucose (through urine).
It is practically feasible for people with type 2 diabetes to lead an active life with limited medical intervention.
A genetic flaw could explain why people suffering from type 2 diabetes have a higher risk of developing cancer. Related:Pesticides are the silent killers of farmersReduce the use of pesticides to protect the health of farmers. West is an online newspaper aimed at providing the latest breaking news on welfare policies. Your skin: A window to your healthSkin problems are often the first sign of serious underlying health problems.
NHS National Genetics Education & Development Centre - Tuberous Sclerosis Complex (TSC). To provide even greater transparency and choice, we are working on a number of other cookie-related enhancements.
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. This condition can occur in a person gradually, over the years and the person may not even realize it until something major affects the health. It is a common sight that people visit their doctor for some other problem and return with the diagnosis of the second stage diabetes. The main cause of this type of diabetes is believed to be insufficient production of insulin or the insulin resistance. However, there is also a popular paradox related to obesity and diabetes that suggests that people who maintain a normal body weight are also at a high risk of developing the insulin resistant diabetes, popularly known as the second stage diabetes.


It is very important to be active in order to stay fit and rule out the chances of developing diabetes. If a person has a family history of parents or siblings with diabetes, then it is very likely that the person may also develop diabetes over the years. Many people are not aware of the risk factors and complications which type 2 diabetes mellitus can bring along with, both in the short and long run.
Consequently, glucose (sugar) cannot get into the body’s cells and their functioning gets impaired.
Many of them can be controlled when you know what puts your health at risk for the illness and the adverse effects which are likely to come.
It may create an overwhelming reaction creating apprehensiveness of the long-term health outcomes and effects on everyday life. This damage can also appear as atherosclerosis, or hardening of the large arteries, making way for heart attack and stroke. Type 2 diabetes can also reduce life expectancy by about 10 years and can be especially concerning for the health and well being of children. Severe illness may develop into a life-threatening complication. Type 2 diabetes, also referred to as non-insulin dependent diabetes, can pose problems in the short run also. Some people may even not remain drug-dependant if they bring in favorable lifestyle changes. In their new study, published in Nature Genetics, researchers from Imperial College London and CNRS in France, suggest that DNA mutations, called clonal mosaic events (CMEs), may be the cause, resulting in extra copies or missing chromosomes which increase cancer risk. Butterfly rashA butterfly rash across the face is often the first sign of lupus, but don't jump to conclusions.
Jorizzo, professor and founding chair of dermatology, Wake Forest University, Winston-Salem, USA. It is intended for general information purposes only and does not address individual circumstances. 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.
Many times, other factors such as genetics and sedentary lifestyle also combines to cause the second stage diabetes. Fat- rich diet and lack of exercise are some of the main reasons that can lead to obesity, eventually causing second stage diabetes.
You must also watch your diet, and try to include fresh vegetables and fruits in your regular diet to stay healthy. In this condition, the body is unable to use this important hormone, insulin to help transport glucose to different parts of the body, so that the body could use it as fuel.
Being diagnosed with diabetes may not only affect you but your loved ones as well who now need to be aware of your additional medical and non-medical needs in living a healthy life. Weight management is an important aspect of managing and living with type 2 diabetes as it promotes the body to utilize insulin appropriately.
Indeed, by involving 7,659 individuals in their analysis, they found a significant association between CME occurrence and type 2 diabetes (T2D), stronger in the non-obese participants with T2D. It is not a substitute for professional medical advice, diagnosis or treatment and should not be relied on to make decisions about your health. 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].
This leads to abnormal build up of sugar content in the blood stream and causes the second stage diabetes.
Even though type 2 diabetes is the form affecting most people suffering from diabetes, it is possible to lead a healthy and active life with minimum complications with the right resources like appropriate information and support.
In CME carriers, an increase in the percentage of abnormal cells over 6 years was found. The finding could partly explain why people with type 2 diabetes are more likely to get blood cancers and help identify those who have higher risk of developing leukemia, in order to start earlier mild therapies. Never ignore professional medical advice in seeking treatment because of something you have read on the BootsWebMD Site. Pyruvate then enters the mitochondria and is decarboxylated to acetyl-CoA, which enters the tricarboxylic acid cycle. 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. Rarely, if it occurs in other parts of the body such as the hands or lips, it may indicate an internal malignant cancer.
The ?-ketoglutarate is oxidised to succinyl-CoA in a reaction catalysed by ?-ketoglutarate dehydrogenase.
Leg plaque: Red on edge, gold in centreNecrobiosis lipoidica is an inflammatory skin condition.
Succinyl-CoA synthase then catalyses the conversion of succinyl-CoA to succinate, with the concomitant phosphorylation of GDP to GTP.
It may occur with inflammatory conditions such as inflammatory bowel disease, rheumatoid arthritis and sarcoid. Very often it is associated with diabetes, when it is called necrobiosis lipoidica diabetica, and often means the underlying diabetes may have damaged the blood vessels in the eyes and kidneys.
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].
Itchy, violet bumps on wristLichen planus is a rash made up of reddish-purple, flat-topped bumps that may be very itchy. It usually appears on the wrists or ankles, but may appear on the lower back, neck, arms, legs and genitals. 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. Flesh coloured, orange-peel patches on backShagreen patches are flesh-coloured lesions on the lower back that have the texture of orange peel.
Oxaloacetate is converted by cytosolic malate dehydrogenase to malate before being converted to pyruvate by malic enzyme. They often occur with other skin signs: red or brown acne-like bumps spreading across the cheeks and nose, and ash-leaf spots of under-pigmented skin, most often on the trunk, that are oval at one end and pointy at the other.
These are signs of a rare genetic disease called tuberous sclerosis that causes benign tumours to grow in the brain and other vital organs. Tripe palmsTripe palms describes a skin condition in which the skin of the palm becomes thick and velvety-white with pronounced folds in the lines of the hand. The NADPH oxidase complex in the plasma membrane is also activated through protein kinase C, which is activated by fatty acid derived signalling molecules.
If tripe palms is accompanied by acanthosis nigricans, it's most likely to be stomach cancer. 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]. If tripe palms is not accompanied by acanthosis nigricans, then lung cancer is usually responsible. 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. Hardening of skin in extremities, ‘wooden’ hands and feetNephrogenic systemic fibrosis starts as a brown discolouration and indentation of the lower arms and legs. 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.
Researchers have found that the gadolinium contrast agent used during MRI examinations triggers this condition in some patients with kidney failure.
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]. Scaly rash on buttocks, red tongueFortunately, necrolytic migratory erythema is quite rare.


Several lines of evidence indicated that there is no hyperglycemia without beta-cell dysfunction [13,14].
It's a red, blistering rash that crusts over sometimes with small erosions of the skin, usually seen in elderly patients. 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].
It tends to start in the fold of the buttocks or genitals but can be elsewhere on the body.
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]. Not all skin conditions are scaryMany skin conditions do not indicate that anything else is wrong with you. For example, granuloma annulare is raised, reddish or flesh-coloured bumps forming ring patterns on the hands and feet.
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. It usually goes away within a few months and usually doesn't mean anything is wrong with you.
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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