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Pathogenesis Of Type 2 Diabetes Mellitus Leahy

Pathogenesis Of Type 2 Diabetes Mellitus

Pathogenesis Of Type 2 Diabetes Mellitus

Part of the Contemporary Endocrinology book series (COE) The pathophysiology of type 2 diabetes is complex, with many different elements acting to cause the disease. This review proposes a sequence of events that is based on a careful analysis of the human and animal model literature. It seems certain that a genetic predisposition is needed although, until recently, little was known about specific genetic mutations. Whether the diabetes phenotype then occurs depends on a large number of environmental factors that share an ability to stress the glucose homeostasis system by promoting insulin resistance or worsening -cell function. We propose that a lowered -cell mass through genetic and/or -cell cytotoxic factors is an important predisposing factor for glucose intolerance. As the blood glucose level rises to a minor degree above normal, acquired defects in the glucose homeostasis system occura key early one is an impaired first phase insulin response to a meal that cause the blood glucose level to rise further into the prediabetes range. This increase in glycemia, perhaps in concert with hyperlipidemia, causes additional deterioration in -cell function and, to a smaller extent, resistance, resulting in a blood glucose level that continues to rise to full blown diabetes. This sequence provides insight into prevention and treatment of type 2 diabetes. One can modify predisposing environmental factors, although that is not easily done. Alternatively, one expects that, as the molecular basis for the organ dysfunctions are discovered (-cell dysfunction and death, and muscle and hepatic insulin resistance), novel therapies will be developed that target those defects. -Cell dysfunctioninsulin resistanceglucose toxicitylipotoxicity-cell apoptosis This is a preview of subscripti Continue reading >>

Pathogenesis Of Type 2 Diabetes Mellitus

Pathogenesis Of Type 2 Diabetes Mellitus

Part of the Contemporary Endocrinology book series (COE) The pathophysiology of type 2 diabetes is complex, with many different elements acting to cause the disease. This review proposes a sequence of events that is based on a careful analysis of the human and animal model literature. It seems certain that a genetic predisposition is needed although, until recently, little was known about specific genetic mutations. Whether the diabetes phenotype then occurs depends on a large number of environmental factors that share an ability to stress the glucose homeostasis system by promoting insulin resistance or worsening -cell function. We propose that a lowered -cell mass through genetic and/or -cell cytotoxic factors is an important predisposing factor for glucose intolerance. As the blood glucose level rises to a minor degree above normal, acquired defects in the glucose homeostasis system occura key early one is an impaired first phase insulin response to a meal that cause the blood glucose level to rise further into the prediabetes range. This increase in glycemia, perhaps in concert with hyperlipidemia, causes additional deterioration in -cell function and, to a smaller extent, resistance, resulting in a blood glucose level that continues to rise to full blown diabetes. This sequence provides insight into prevention and treatment of type 2 diabetes. One can modify predisposing environmental factors, although that is not easily done. Alternatively, one expects that, as the molecular basis for the organ dysfunctions are discovered (-cell dysfunction and death, and muscle and hepatic insulin resistance), novel therapies will be developed that target those defects. -Cell dysfunctioninsulin resistanceglucose toxicitylipotoxicity-cell apoptosis This is a preview of subscripti Continue reading >>

Pathogenesis Of Type 2 Diabetes Mellitus.

Pathogenesis Of Type 2 Diabetes Mellitus.

1. Arch Med Res. 2005 May-Jun;36(3):197-209. Pathogenesis of type 2 diabetes mellitus. (1)University of Vermont College of Medicine, Burlington, VT 05405, USA. [email protected] The pathological sequence for type 2 diabetes is complex and entails manydifferent elements that act in concert to cause that disease. This reviewproposes a sequence of events and how they interact by a careful analysis of the human and animal model literature. A genetic predisposition must exist, although to date very little is known about specific genetic defects in this disease.Whether the diabetes phenotype will occur depends on many environmental factorsthat share an ability to stress the glucose homeostasis system, with the current explosion of obesity and sedentary lifestyle being a major cause of the worldwidediabetes epidemic. We also propose that a lowered beta-cell mass either throughgenetic and/or beta-cell cytotoxic factors predisposes for glucose intolerance.As the blood glucose level rises even a small amount above normal, then acquired defects in the glucose homeostasis system occur--initially to impair the betacell's glucose responsiveness to meals by impairing the first phase insulinresponse--and cause the blood glucose level to rise into the range of impairedglucose tolerance (IGT). This rise in blood glucose, now perhaps in concert with the excess fatty acids that are a typical feature of obesity and insulinresistance, cause additional deterioration in beta-cell function along withfurther insulin resistance, and the blood glucose levels rise to full-blowndiabetes. This sequence also provides insight into how to better prevent or treattype 2 diabetes, by studying the molecular basis for the early defects, anddeveloping targeted therapies against them. Continue reading >>

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An Error Occurred Setting Your User Cookie

An Error Occurred Setting Your User Cookie This site uses cookies to improve performance. If your browser does not accept cookies, you cannot view this site. There are many reasons why a cookie could not be set correctly. Below are the most common reasons: You have cookies disabled in your browser. You need to reset your browser to accept cookies or to ask you if you want to accept cookies. Your browser asks you whether you want to accept cookies and you declined. To accept cookies from this site, use the Back button and accept the cookie. Your browser does not support cookies. Try a different browser if you suspect this. The date on your computer is in the past. If your computer's clock shows a date before 1 Jan 1970, the browser will automatically forget the cookie. To fix this, set the correct time and date on your computer. You have installed an application that monitors or blocks cookies from being set. You must disable the application while logging in or check with your system administrator. This site uses cookies to improve performance by remembering that you are logged in when you go from page to page. To provide access without cookies would require the site to create a new session for every page you visit, which slows the system down to an unacceptable level. This site stores nothing other than an automatically generated session ID in the cookie; no other information is captured. In general, only the information that you provide, or the choices you make while visiting a web site, can be stored in a cookie. For example, the site cannot determine your email name unless you choose to type it. Allowing a website to create a cookie does not give that or any other site access to the rest of your computer, and only the site that created the cookie can read it. Continue reading >>

Using Prandial Insulin To Achieve Glycemic Control In Type 2 Diabetes

Using Prandial Insulin To Achieve Glycemic Control In Type 2 Diabetes

Using prandial insulin to achieve glycemic control in type 2 diabetes J Fam Pract. 2007 September;56(9):735-741 Dr Dailey has been on the speakers bureau for Amylin Pharmaceuticals, Inc; Bristol-Myers Squibb Company; Eli Lilly and Company; GlaxoSmithKline; Merck & Co, Inc; Merck KGaA; Novartis Pharmaceuticals Corporation; Pfizer Inc; and Sanofi-Aventis US. He also has been an investigator for Amylin Pharmaceuticals, Inc; Becton, Dickinson and Company; Bristol-Myers Squibb Company; Eli Lilly and Company; Forest Pharmaceuticals, Inc; GlaxoSmithKline; Merck & Co, Inc; Novartis Pharmaceuticals Corporation; Novo Nordisk Pharmaceuticals, Inc; Pfizer Inc; Pharmacia; Roche; Sanofi-Aventis US; Schering-Plough; and Takeda Pharmaceuticals North America, Inc. Dr Dailey is also an occasional consultant for Amylin Pharmaceuticals, Inc; Bristol-Myers Squibb Company; Eli Lilly and Company; GlaxoSmithKline; Merck & Co, Inc; Novo Nordisk Pharmaceuticals, Inc; Pfizer Inc; and Sanofi-Aventis US. 1. Bonora E, Corrao G, Bagnardi V, et al. Prevalence and correlates of post-prandial hyperglycaemia in a large sample of patients with type 2 diabetes mellitus. Diabetologia 2006;49:846-854. 2. Tominaga M, Eguchi H, Manaka H, Igarashi K, Kato T, Sekikawa A. Impaired glucose tolerance is a risk factor for cardiovascular disease, but not impaired fasting glucose. The Funagata Diabetes Study. Diabetes Care 1999;22:920-924. 3. The DECODE study group on behalf of the European Diabetes Epidemiology Group. Glucose tolerance and mortality: comparison of WHO and American Diabetes Association diagnostic criteria. Lancet 1999;354:617-621. 4. Decode Study Group. Is the current definition for diabetes relevant to mortality risk from all causes and cardiovascular and noncardiovascular diseases? Diabetes Care 20 Continue reading >>

Pathogenesis Of Type 2 Diabetes

Pathogenesis Of Type 2 Diabetes

All APS members receive FREE access to Comprehensive Physiology. Use your APS credentials to log in from the APS website. Source: Supplement 21: Handbook of Physiology, The Endocrine System, The Endocrine Pancreas and Regulation of Metabolism 1.3Other Abnormalities in Insulin Secretion in T2DM 2Mechanisms of Impaired Insulin Secretion 2.3Other Mechanisms of Impaired Insulin Secretion in T2DM 3Impaired Insulin Secretion: Primary Genetic Defect Responsible for Type 2 Diabetes 3.4Subjects with History of Gestational Diabetes Mellitus 4Hypersecretion of Insulin as the Cause of Type 2 Diabetes: A New Hypothesis 6.1Site of Insulin Resistance in Type 2 Diabetes 6.2Fasting Hyperglycemia: Role of Pancreas, Muscle and Liver 6.3Postprandial Hyperglycemia: Lessons from the Oral Glucose Tolerance Test 7Dynamic Interaction Between Insulin Sensitivity and Insulin Secretion in Type 2 Diabetes Mellitus 8Cellular Mechanisms of Insulin Resistance in Type 2 Diabetes 8.2Insulin Receptor/Insulin Receptor Signal Transduction Defects 9Metabolic, Hemodynamic, Endocrine, and Cytokine Abnormalities in Type 2 Diabetes Mellitus 9.2Lipid Oxidation and Insulin Resistance 9.3Skeletal Muscle Capillary Density, Fiber Type and Endothelial Transport 9.5Amylin and Calcitonin GeneRelated Peptide 9.7Acquired Determinants of Insulin Resistance 10Summary of Insulin Resistance in Type 2 Diabetes Mellitus 12Pathogenesis of Type 2 Diabetes Mellitus: Summary and Synthesis 12.1Primary Defect in Insulin Sensitivity 12.2Primary Defect in Insulin Secretion? 12.3Combined Defects in Insulin Sensitivity and Insulin Secretion Schematic representation of glucose production and glucose utilization in the normal human in the postabsorptive state [Drawn from data presented in DeFronzo et al. , , and .] Relationship between f Continue reading >>

Which Comes First In Non—insulin-dependent Diabetes Mellitus: Insulin Resistance Or Beta-cell Failure? Both Come First

Which Comes First In Non—insulin-dependent Diabetes Mellitus: Insulin Resistance Or Beta-cell Failure? Both Come First

The curious physician trying to understand the pathogenesis of non—insulin-dependent diabetes mellitus (NIDDM) has every reason to be mystified by the barrage of conflicting claims about the primacy of beta-cell failure and insulin resistance. How can the argument go on for so long without a clear answer? Probably because we keep trying to view NIDDM as being simpler than it really is, and because we expect that the first identifiable lesion will lead us to the primary cause. Since there is general agreement that a combination of both environmental and genetic forces leads to NIDDM, it is probably counterproductive to think in terms of a primary cause or something that comes first. The major environmental problem seems to be our modern obesity-promoting lifestyle of limited physical activity and abundant food. Not only is obesity associated with insulin resistance, but sedentary behavior by itself leads to reduced insulin action on muscle. Continue reading >>

Type 2 Diabetes Mellitus:

Type 2 Diabetes Mellitus:

Verwachte levertijd ongeveer 8 werkdagen . In this practical book, the authors of each chapter have synthesized the currently available evidence regarding specific issues in diabetes care. The chapters have been written by an interdisciplinary team of scientists and medical professionals. Such an approach emphasizes the need for collaboration in the care of any individual with diabetes and in the effort to find new therapies for the... Toon volledige samenvatting In this practical book, the authors of each chapter have synthesized the currently available evidence regarding specific issues in diabetes care. The chapters have been written by an interdisciplinary team of scientists and medical professionals. Such an approach emphasizes the need for collaboration in the care of any individual with diabetes and in the effort to find new therapies for the disease. This reference provides practical guidance in a single resource. 2. Pathogenesis of Type 2 Diabetes Mellitus/ Leahy 3. Metabolic Mechanisms of Muscle Insulin Resistance/ Mudio 4. Fat Metabolism in Insulin Resistance and Type 2 Diabetes 5. Detection and Diagnosis of Type 2 Diabetes/ Vella 6. Therapies for Delay or Prevention of Type 2 Diabetes/ Bethel 8. Medical Nutrition Therapy in Type 2 Diabetes/ Maryniuk 9. Exercise as an Effective Treatment for Type 2 Diabetes/ Houmard 10. Non-Insulin Pharmacological Therapies/ Lingvay 11. The Transition from Oral Agents to Combination Insulin/Oral Therapy/ Riddle 12. Intensive Insulin Therapy in T2DM/ Edelman 13. Hypoglycemia in Type 2 Diabetes / Cryer 14. Type 2 Diabetes and Concomitant Illness: The Prepared Practice/ Dungan 15. Adherence to Practice Guidelines for People with Diabetes Mellitus / Blonde 16. Treatment of Hypertension in Type 2 Diabetes/ Goff 17. Lipoproteins i Continue reading >>

Basal Insulin Therapy In Type 2 Diabetes

Basal Insulin Therapy In Type 2 Diabetes

Abstract Patients with type 2 diabetes mellitus are usually treated initially with oral antidiabetic agents, but as the disease progresses, most patients eventually require insulin to maintain glucose control. Optimal insulin therapy should mimic the normal physiologic secretion of insulin and minimize the risk of hypoglycemia. This article discusses the role of insulin therapy in patients with type 2 diabetes, emphasizing long-acting insulin agents designed to approximate physiologic basal insulin secretion and provide control over fasting plasma glucose. Clinical trials of recently developed long-acting insulins are reviewed herein, with emphasis on studies that combined basal insulin with oral agents or with short-acting insulins in a basal-bolus approach. The normal physiologic pattern of insulin secretion by pancreatic β cells consists of a sustained basal insulin level throughout the day, superimposed after meals by relatively large bursts of insulin that slowly decay over 2 to 3 hours (bolus insulin). Basal support with long-acting insulin is a key component of basal-bolus therapy for patients with diabetes who require insulin with or without the addition of oral agents. Newer long-acting agents such as insulin glargine provide a steadier and more reliable level of basal insulin coverage and may have significant advantages over traditional long-acting insulins as part of a basal-bolus treatment strategy. Continue reading >>

Reexamining The Multifaceted Defects Underlying The Pathophysiology Of Type 2 Diabetes (slides With Transcript)

Reexamining The Multifaceted Defects Underlying The Pathophysiology Of Type 2 Diabetes (slides With Transcript)

Reexamining the Multifaceted Defects Underlying the Pathophysiology of Type 2 Diabetes (Slides with Transcript) This activity has been designed to meet the educational needs of physicians and other health care professionals interested in learning more about novel mechanisms for achieving glycemic control in patients with type 2 diabetes. Our increased appreciation for the underlying pathophysiology of type 2 diabetes has led to the development of novel therapeutics that improve glycemic control and islet cell function through the modulation of incretin hormones. Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are 2 principal incretin hormones that promote glucose homeostasis through glucose-dependent regulation of insulin and glucagon. Both hormones are rapidly inactivated by the enzyme dipeptidyl peptidase-4 (DPP-4). Novel therapeutic strategies, including the administration of long-acting GLP-1 receptor agonists and, alternatively, preventing the inactivation of GLP-1 and GIP through selective inhibition of DPP-4, have been shown to stimulate insulin secretion from pancreatic beta cells and inhibit glucagon secretion from pancreatic alpha cells in a glucose-dependent manner. Incretin-based therapies have also been shown to promote beta-cell proliferation, inhibit apoptosis, and expand beta-cell mass in experimental animal models of diabetes. This activity will review the role of incretin hormones in improving islet cell function and promoting glucose homeostasis, and address the role of incretin-based therapeutics, alone and as combination therapy, in the management of type 2 diabetes. Upon completion of this activity, participants should be able to: Describe the interrelated pathophysiologic abnormalities that contribute to the Continue reading >>

Consensus Statement: Targeting Beta-cell Function Early

Consensus Statement: Targeting Beta-cell Function Early

Home Cell Science Consensus Statement: Targeting Beta-Cell Function Early Consensus Statement: Targeting Beta-Cell Function Early Targeting Beta-Cell Function Early in the Course of Therapy for Type 2 Diabetes Mellitus Excerpt from a consensus statement recently published in the Journal of Clinical Endocrinology & Metabolism (JCEM) Traditionally, Type 2 diabetes mellitus (T2DM) is viewed as a progressive disease. Pathogenesis is complex, characterized by genetic predisposition thattogether with metabolic abnormalities associated with body-weight gain, defective insulin secretion and action, and elevated endogenous glucose productioneventually compromise glucose homeostasis (1). Evidence from both human and animal studies suggests that T2DM is characterized by decreased functional -cell mass that cannot adapt insulin secretion to compensate for increasing insulin resistance driving the development of overt T2DM (2, 3). -cell function continues declining progressively despite treatment with anti-diabetic medications as well, as highlighted in the 1995 United Kingdom Prospective Diabetes Study (4). Accumulating evidence suggests this decline may be slowed or even reversed, particularly in early stages of disease (5). Furthermore, new therapeutic classes of diabetes medications act to improve -cell function, thus potentially altering the course of the disease. The precise role these new therapies might play in treating T2DM, however, has not yet been fully addressed. In fact, despite the primary and pivotal role that -cells appear to play in disease development and progression, current clinical practice remains heavily focused on insulin resistance. FIG. 1. Proposed sequence of the key pathological features of T2DM. Click to enlarge . [Adapted from J.L.Leahy: Arch Med Res Continue reading >>

Pathophysiology | Beta Cells In Diabetes

Pathophysiology | Beta Cells In Diabetes

Rhodes, Christopher J; White, Morris F; Leahy, John L; Kahn, Steven E Diabetes; 2013 Jul;62(7):2157-63. PMID: 23801714 Endocrine reviews; 2012 Apr;33(2):187-215. PMID: 22323472 Dhruv K. Singh, Peter Winocour & Ken Farrington Nature reviews. Immunology; 2011 Feb;11(2):98-107. PMID: 21233852 Current opinion in lipidology; 2011 Feb;22(1):26-32. PMID: 21102330 Mssig, K; Staiger, H; Machicao, F; Hring, H-U; Fritsche, A Diabetologia; 2010 Nov;53(11):2289-97. PMID: 20714888 Leahy, Jack L; Hirsch, Irl B; Peterson, Kevin A; Schneider, Doron The Journal of clinical endocrinology and metabolism; 2010 Sep;95(9):4206-16. PMID: 20739389 Advances in experimental medicine and biology; 2010;654:391-419. PMID: 20217507 Saxena, Richa; Hivert, Marie-France; Langenberg, Claudia; Tanaka, Toshiko; Pankow, James S; Vollenweider, Peter; Lyssenko, Valeriya; Bouatia-Naji, Nabila; Dupuis, Jose; Jackson, Anne U; Kao, W H Linda; Li, Man; Glazer, Nicole L; Manning, Alisa K; Luan, J Nature genetics; 2010 Feb;42(2):142-8. PMID: 20081857 Continue reading >>

Diabetes Defined: Pathophysiology

Diabetes Defined: Pathophysiology

Type 1a diabetes mellitus or immune-mediated diabetes, more commonly known as Type 1 diabetes,comprises only 5% to 10% of all diabetes cases worldwide.2 However, it is one of the most commonchronic childhood disease states. Idiopathic Type 1 diabetes or Type 1b diabetes mellitus occurs whenpatients with no evidence of autoimmunity experience complete insulin deficiency; this type will not bediscussed in great detail in this review.8 Type 1 diabetes was previously known as insulin-dependentdiabetes or juvenile-onset diabetes and nearly 500,000 children live with it and almost 79,000 developthe disease every year worldwide.1 While this impact is very small compared with the number ofindividuals with Type 2 diabetes, the incidence of Type 1 diabetes is increasing by approximately 3.2%per year.9 The reasons for the upward trend are not clear, but it is important to remember thatindividuals diagnosed with Type 1 diabetes can live well into their older adult years if the disease ismanaged appropriately. Type 1 diabetes usually presents in children and young adults. For individuals younger than 20 years ofage, Type 1 diabetes accounts for the majority of new diabetes cases diagnosed in the U.S.10 The age ofpresentation peaks at the following 2 distinctive points: one peak occurs from 4 to 6 years of age andthe other peaks in early puberty (i.e., 10 to 14 years of age).11 Overall, roughly 45% of children with Type1 diabetes are diagnosed when they are younger than 10 years of age; however, adults comprise one-quarter of all Type 1 diabetes diagnoses.2 Type 1 diabetes can present in several different ways. Children tend to present with the abrupt onset ofpolydipsia, polyuria, weight loss, and hyperglycemia.12 Hyperglycemia sufficient enough to be classifiedas diabetes is when g Continue reading >>

The Influence Of Ethnicity On The Development Of Type 2 Diabetes Mellitus In Women With Gestational Diabetes: A Prospective Study And Review Of The Literature

The Influence Of Ethnicity On The Development Of Type 2 Diabetes Mellitus In Women With Gestational Diabetes: A Prospective Study And Review Of The Literature

The Influence of Ethnicity on the Development of Type 2 Diabetes Mellitus in Women with Gestational Diabetes: A Prospective Study and Review of the Literature 1Diabetes and Transcription Factors Group, Garvan Institute of Medical Research, Darlinghurst, Sydney, NSW 2010, Australia 2Faculty of Medicine, University of Sydney, Sydney, NSW 2006, Australia 3Department of Diabetes and Endocrinology, Westmead Hospital, Weatmead, NSW 2145, Australia 4St Vincents Clinical School, University of NSW, Sydney, NSW 2010, Australia Received 20 January 2012; Accepted 15 February 2012 Academic Editors: C. Anderwald, B. Larijani, and A. Saxe Copyright 2012 Christian M. Girgis et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. S. Wild, G. Roglic, A. Green, R. Sicree, and H. King, Global prevalence of diabetes: estimates for the year 2000 and projections for 2030, Diabetes Care, vol. 27, no. 5, pp. 10471053, 2004. View at Publisher View at Google Scholar View at Scopus W. Yang, J. Lu, J. Weng et al., Prevalence of diabetes among men and women in China, New England Journal of Medicine, vol. 362, no. 12, pp. 10901101, 2010. View at Publisher View at Google Scholar View at Scopus R. Pradeepa, R. Deepa, and V. Mohan, Epidemiology of diabetes in Indiacurrent perspective and future projections, Journal of the Indian Medical Association, vol. 100, no. 3, pp. 144148, 2002. View at Google Scholar View at Scopus J. L. Leahy and R. E. Pratley, What is type 2 diabetes mellitus? crucial role of maladaptive changes in beta cell and adipocyte biology, Translational Endocrinology and Metabolism, vol. 2, no. 1, pp. 942, 2011. View at Go Continue reading >>

Mechanisms Of Beta Cell Compensation And Failure Leahy, John L. University Of Vermont & St Agric College, Burlington, Vt, United States

Mechanisms Of Beta Cell Compensation And Failure Leahy, John L. University Of Vermont & St Agric College, Burlington, Vt, United States

Mechanisms of Beta cell Compensation and Failure A key pathogenic feature of type 2 diabetes is loss of the beta-cell compensation to the insulin resistance that occurs in this disease. The biochemical and molecular nature of this beta-cell failure are poorly known, in part because of lack of animal models that faithfully reproduce the natural history of the human disease. This proposal makes use of a newly developed rat model, the 60% pancreatectomy Zucker rat that incorporates the characteristic features of human adipogenic diabetes - obesity, insulin resistance, and hyperlipidemia. They are characterized by a 3-week period of relative normoglycemia after the partial pancreatectomy (compensation phase) that is followed by the onset of beta-cell dysfunction and mild hyperglycemia (decompensation phase). We will use this model to test the hypothesis of this application that enhanced then impaired a-cell anaplerosis and lipid partitioning are the mechanistic basis for the beta-cell compensation and subsequent beta-cell failure in these rats. A notable aspect of this application is it stems as a joint effort from the laboratories of Drs. Jack Leahy (Burlington, VT) and Marc Prentki (Montreal, Canada) who have complimentary research expertise in the fields of beta cell anaplerosis/lipid partitioning and the beta cell failure in rodent models of type 2 diabetes. Aim 1 will determine the cellular mechanisms and signaling pathways for beta-cell compensatory growth or loss of beta-cell mass in the 60% Px ZF rat model at different stages during the progression to diabetes. Aim 2 will test the hypothesis that the mechanism of beta-cell decompensation in the 60% Px ZF rat model is related to failure of compensatory enhanced anaplerosis and lipid signaling processes. Aim 3 will t Continue reading >>

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