Molecular Mechanism Of Insulin Resistance In Type 2 Diabetes Mellitus: Role Of The Insulin Receptor Variant Forms
Molecular mechanism of insulin resistance in type 2 diabetes mellitus: role of the insulin receptor variant forms University of CatanzaroMagna, Graecia, Italy c/o Dipartimento di Medicina Interna, Universit di Roma Tor Vergata, Via Tor Vergata 135, 00133 Rome, Italy. Search for more papers by this author University of CatanzaroMagna, Graecia, Italy c/o Dipartimento di Medicina Interna, Universit di Roma Tor Vergata, Via Tor Vergata 135, 00133 Rome, Italy. Search for more papers by this author Please review our Terms and Conditions of Use and check box below to share full-text version of article. I have read and accept the Wiley Online Library Terms and Conditions of Use. Use the link below to share a full-text version of this article with your friends and colleagues. Learn more. Get access to the full version of this article.View access options below. You previously purchased this article through ReadCube. View access options below. Logged in as READCUBE_USER. Log out of ReadCube . Type 2 diabetes is a heterogeneous and polygenic disorder resulting from interaction of genetic factors with environmental influences. Numerous candidate genes for insulin signaling proteins have been screened, but no single major susceptibility gene for type 2 diabetes has been identified. Due to its pivotal role in insulin action, the insulin receptor was considered a plausible candidate gene. The insulin receptor exists in two isoforms differing by the absence (Ex11) or presence (Ex11+) of a 12 amino acid sequence in the COOHterminus of the subunit, as a consequence of alternative splicing of exon 11. The Ex11 binds insulin with twofold higher affinity than the Ex11+. This difference is paralleled by a decreased sensitivity for metabolic actions of insulin. Some, but not all, studies have Continue reading >>
- Effects of Insulin Plus Glucagon-Like Peptide-1 Receptor Agonists (GLP-1RAs) in Treating Type 1 Diabetes Mellitus: A Systematic Review and Meta-Analysis
- Resistance Training for Diabetes Prevention and Therapy: Experimental Findings and Molecular Mechanisms
- Early-onset and classical forms of type 2 diabetes show impaired expression of genes involved in muscle branched-chain amino acids metabolism
Molecular Mechanisms In Autoimmune Type 1 Diabetes: A Critical Review.
1. Clin Rev Allergy Immunol. 2014 Oct;47(2):174-92. doi: 10.1007/s12016-014-8422-2. Molecular mechanisms in autoimmune type 1 diabetes: a critical review. (1)Diabetes Center, 2nd Xiangya Hospital, and Institute of Metabolism and Endocrinology, Key Laboratory of Diabetes Immunology, Ministry of Education, Central South University, Changsha, Hunan, 410011, China. Erratum in Clin Rev Allergy Immunol. 2014 Oct;47(2):258. Autoimmune type 1 diabetes is characterized by selective destruction ofinsulin-secreting beta cells in the pancreas of genetically susceptibleindividuals. The mechanisms underlying the development of type 1 diabetes are notfully understood. However, a widely accepted point is that type 1 diabetes iscaused by a combination of genetic and environmental factors. Although most type 1 diabetes patients do not have a family history, genetic susceptibility doesplay a vital role in beta cell autoimmunity and destruction. Human leukocyteantigen (HLA) regions are the strongest genetic determinants, which cancontribute 40-50 % of the genetic risk to type 1 diabetes. Other genes, includingINS also contribute to disease risk. The mechanisms of the susceptible genes intype 1 diabetes may relate to their respective roles in antigen presentation,beta cell autoimmunity, immune tolerance, and autoreactive T cell response.Environmental susceptibility factors also contribute to the risk of developingtype 1 diabetes. From an epigenetic standpoint, the pathologic mechanismsinvolved in the development of type 1 diabetes may include DNA methylation,histone modification, microRNA, and molecular mimicry. These mechanisms may actthrough regulating of gene expression, thereby affecting the immune systemresponse toward islet beta cells. One of the characteristics of type 1 diabetesis Continue reading >>
- Resistance Training for Diabetes Prevention and Therapy: Experimental Findings and Molecular Mechanisms
- Relative contribution of type 1 and type 2 diabetes loci to the genetic etiology of adult-onset, non-insulin-requiring autoimmune diabetes
- Drug to Reverse Type 2 Diabetes Passes Critical Test in Mice
The Pathogenesis And Pathophysiology Of Type 1 And Type 2 Diabetes Mellitus
Vol. 4(4), pp. 46-57, September, 2013 DOI 10.5897/JPAP2013.0001 ISSN 2I41-260X © 2013 Academic Journals Journal of Physiology and Pathophysiology Review The pathogenesis and pathophysiology of type 1 and type 2 diabetes mellitus Ozougwu, J. C.1*, Obimba, K. C.2, Belonwu, C. D.3, and Unakalamba, C. B.4 Physiology and Biomedical Research Unit, Department of Biological Sciences, College of Basic and Applied Sciences, Rhema University Aba, Abia State, Nigeria. 2 Department of Biochemistry, School of Science, Federal University of Technology Owerri. Imo State. Nigeria. 3 Department of Biochemistry, Faculty of Chemical Sciences, University of Portharcourt. Rivers State. Nigeria. 4 Department of Zoology and Environmental Biology, University of Nigeria, Nsukka, Enugu state, Nigeria. The aim of this paper is to review the information on type 1 and type 2 diabetes with emphasis on its etiology, pathogenesis and pathophysiology via literature review. Diabetes is a group of metabolic disorders characterized by a chronic hyperglycemic condition resulting from defects in insulin secretion, insulin action or both. Type 1 diabetes is the result of an autoimmune reaction to proteins of the islets cells of the pancreas while type 2 diabetes is caused by a combination of genetic factors related to impaired insulin secretion, insulin resistance and environmental factors such as obesity, overeating, lack of exercise and stress, as well as aging. The pathogenesis of selective β-cell destruction within the islet in type 1 diabetes mellitus is difficult to follow due to marked heterogeneity of the pancreatic lesions. At the onset of overt hyperglycemia, a mixture of pseudoatrophic islets with cells producing glycogen, somatostatin and pancreatic polypeptide, normal islets and islets cont Continue reading >>
Diabetes: Mechanism, Pathophysiology And Management-a Review
Anees A Siddiqui1*, Shadab A Siddiqui2, Suhail Ahmad, Seemi Siddiqui3, Iftikhar Ahsan1, Kapendra Sahu1 Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi (INDIA)-110062. School of Pharmacy, KIET, Ghaziabad U.P. SGC college of Pharmacy, Baghpat(UP) Corresponding Author:Anees A Siddiqui E-mail: [email protected] Received: 20 February 2011 Accepted: 02 May 2011 Citation: Anees A Siddiqui, Shadab A Siddiqui, Suhail Ahmad, Seemi Siddiqui, Iftikhar Ahsan, Kapendra Sahu “Diabetes: Mechanism, Pathophysiology and Management-A Review” Int. J. Drug Dev. & Res., April-June 2013, 5(2): 1-23. Copyright: © 2013 IJDDR, Anees A Siddiqui et al. This is an open access paper distributed under the copyright agreement with Serials Publication, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Related article at Pubmed, Scholar Google Visit for more related articles at International Journal of Drug Development and Research The prevalence of diabetes is rapidly rising all over the globe at an alarming rate. Over the last three decades, the status of diabetes has been changed, earlier it was considered as a mild disorder of the elderly people. Now it becomes a major cause of morbidity and mortality affecting the youth and middle aged people. According to the Diabetes Atlas 2006 published by the International Diabetes Federation, the number of people with diabetes in India currently around 40.9 million is expected to rise to 69.9 million by 2025 unless urgent preventive steps are taken. The main force of the epidemic of diabetes is the rapid epidemiological transition associated with changes in dietary patterns and decreased physical activity a Continue reading >>
Type 1 Diabetes: Pathogenesis And Prevention
Go to: Genes: How important are they? Like other organ-specific autoimmune diseases, type 1 diabetes has human leukocyte antigen (HLA) associations, but how well are they understood? The HLA on chromosome 6 was the first locus shown to be associated with the disease by candidate gene studies4,5 and is considered to contribute about half of the familial basis of type 1 diabetes.6,7 Two combinations of HLA genes (or haplotypes) are of particular importance: DR4-DQ8 and DR3-DQ2 are present in 90% of children with type 1 diabetes.8 A third haplotype, DR15-DQ6, is found in less than 1% of children with type 1 diabetes, compared with more than 20% of the general population, and is considered to be protective.9 The genotype combining the 2 susceptibility haplotypes (DR4-DQ8/DR3-DQ2) contributes the greatest risk of the disease and is most common in children in whom the disease develops very early in life.10 First-degree relatives of these children are themselves at greater risk of type 1 diabetes than are the relatives of children in whom the disease develops later.11 Candidate gene studies also identified the insulin gene on chromosome 11 as the second most important genetic susceptibility factor, contributing 10% of genetic susceptibility to type 1 diabetes.12 Shorter forms of a variable number tandem repeat in the insulin promoter are associated with susceptibility to the disease, whereas longer forms are associated with protection.13 Demonstration of increased expression of insulin (mRNA) in the thymus of people with “long” or protective repeats — which suggests more efficient deletion of insulin-specific T cells during induction of central tolerance — provides an attractive potential mechanism for the role of the insulin gene in type 1 diabetes.14,15 Over the last Continue reading >>
What Is Diabetes Mellitus?
Diabetes mellitus is a common disease where there is too much sugar (glucose) floating around in your blood. This occurs because either the pancreas can’t produce enough insulin or the cells in your body have become resistant to insulin. When you eat food, the amount of glucose in your blood skyrockets. That’s because the food you eat is converted into glucose (usable energy for your cells) and enters your blood to be transported to your cells around the body. Special cells in your pancreas sense the increase of glucose and release insulin into your blood. Insulin has a lot of different jobs, but one of its main tasks is to help decrease blood glucose levels. It does this by activating a system which transports glucose from your blood into your cells. It also decreases blood glucose by stimulating an enzyme called glycogen synthase in the liver. This molecule is responsible for making glycogen, a long string of glucose, which is then stored in the liver and used in the future when there is a period of low blood glucose. As insulin works on your body, the amount of glucose in the blood slowly returns to the same level it was before you ate.. This glucose level when you haven’t eaten recently (called fasting glucose) sits around 3.5-6 mmol/L (70-110 mg/dL). Just after a meal, your blood glucose can jump as high as 7.8mmol/L (140 mg/dL) depending on how much and what you ate. There are two types of diabetes mellitus, type 1 and type 2. In both types, your body has trouble transporting sugar from your blood into your cells. This leads to high levels of glucose in your blood and a deficiency of glucose in your cells. The main difference between type 1 and type 2 diabetes mellitus is the underlying mechanisms that cause your blood sugar to stray from the normal range. T Continue reading >>
Mechanisms In Endocrinology: Insulin And Type 1 Diabetes: Immune Connections
MECHANISMS IN ENDOCRINOLOGY: Insulin and type 1 diabetes: immune connections 1INSERM, U986, DeAR Lab Avenir, Saint Vincent de Paul Hospital, 82 Avenue Denfert Rochereau, 75674 Paris Cedex 14, France 2Paris Descartes University, Sorbonne Paris Cit, Facult de Mdecine, Paris, France and 3Assistance Publique Hpitaux de Paris, Service de Diabtologie, Htel Dieu, Paris, France (Correspondence should be addressed to R Mallone at INSERM, U986, DeAR Lab Avenir, Saint Vincent de Paul Hospital; Email: roberto.mallone{at}inserm.fr) Insulin is the hormone produced by pancreatic -cells, with a central role in carbohydrate and fat metabolism. Together with its precursors preproinsulin and proinsulin, insulin is also a key target antigen (Ag) of the autoimmune islet destruction leading to type 1 diabetes. Being recognized by both autoantibodies (aAbs) and autoreactive T cells, insulin plays a triggering role, at least in rodent models, in diabetes pathogenesis. It is expressed not only by -cells but also in the thymus, where it plays a major role in central tolerance mechanisms. We will summarize current knowledge concerning insulin, its role in -cell autoimmunity as initial target Ag, its recognition by aAbs and autoreactive T cells, and the detection of these immune responses to provide biomarkers for clinical trials employing insulin as an immune modulatory agent. Type 1 diabetes (T1D) is one of the most common autoimmune diseases, resulting from the destruction of insulin-producing -cells in the pancreatic islets of Langerhans. At the crossroads between endocrine and immune pathways, insulin is the central actor in this disease. It is the key hormone of glucose metabolism, which is lacking in T1D. At the same time, it is one of the key molecular target antigens (Ags) recognized by Continue reading >>
Type 1 Diabetes Mellitus
Author: Romesh Khardori, MD, PhD, FACP; Chief Editor: George T Griffing, MD more... Type 1 diabetes is a chronic illness characterized by the bodys inability to produce insulin due to the autoimmune destruction of the beta cells in the pancreas. Although onset frequently occurs in childhood, the disease can also develop in adults. [ 1 ] See Clinical Findings in Diabetes Mellitus , a Critical Images slideshow, to help identify various cutaneous, ophthalmologic, vascular, and neurologic manifestations of DM. The classic symptoms of type 1 diabetes are as follows: Other symptoms may include fatigue, nausea, and blurred vision. The onset of symptomatic disease may be sudden. It is not unusual for patients with type 1 diabetes to present with diabetic ketoacidosis (DKA). See Clinical Presentation for more detail. Diagnostic criteria by the American Diabetes Association (ADA) include the following [ 2 ] : A fasting plasma glucose (FPG) level 126 mg/dL (7.0 mmol/L), or A 2-hour plasma glucose level 200 mg/dL (11.1 mmol/L) during a 75-g oral glucose tolerance test (OGTT), or A random plasma glucose 200 mg/dL (11.1 mmol/L) in a patient with classic symptoms of hyperglycemia or hyperglycemic crisis A fingerstick glucose test is appropriate for virtually all patients with diabetes. All fingerstick capillary glucose levels must be confirmed in serum or plasma to make the diagnosis. All other laboratory studies should be selected or omitted on the basis of the individual clinical situation. An international expert committee appointed by the ADA, the European Association for the Study of Diabetes, and the International Diabetes Association recommended the HbA1c assay for diagnosing type 1 diabetes only when the condition is suspected but the classic symptoms are absent. [ 3 ] Screen Continue reading >>
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- Postprandial Blood Glucose Is a Stronger Predictor of Cardiovascular Events Than Fasting Blood Glucose in Type 2 Diabetes Mellitus, Particularly in Women: Lessons from the San Luigi Gonzaga Diabetes Study
- Metabolic surgery for treating type 2 diabetes mellitus: Now supported by the world's leading diabetes organizations
Mechanisms And Therapeutic Targets In Type 2 Diabetes Mellitus - Sciencedirect
Volume 1, Issue 2 , November 2004, Pages 151-157 Author links open overlay panel BrandyPanunti Ali A.Jawa Vivian A.Fonseca Get rights and content The pathogenesis of type 2 diabetes mellitus is multifactorial and complex, and it is influenced by both genetic and environmental factors. This metabolic disorder results from insulin resistance in target tissues and impairment of pancreatic insulin secretion. The purpose of this review is to examine our current understanding of the pathophysiology of type 2 diabetes, identify therapeutic targets, and highlight recent advances in addressing this complex disorder. Daniel J. Rader University of Pennsylvania Medical Center, USA The authors review the pathophysiology of type 2 diabetes mellitus, a condition which is rapidly increasing in prevalence and which is a major risk factor for macro- and microvascular disease. Insulin resistance and impairment of insulin secretion both contribute to the expression of type 2 diabetes, but a detailed understanding of the molecular pathophysiology of type 2 diabetes is gradually being elucidated. Ultimately, this information will undoubtedly lead to new therapies for the prevention and treatment of type 2 diabetes and its complications. Continue reading >>
- Pharmacology and therapeutic implications of current drugs for type 2 diabetes mellitus
- The UK Prospective Diabetes Study (UKPDS): clinical and therapeutic implications for type 2 diabetes
- International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #59: Mechanisms of insulin signal transduction Part 3 of 8
Classification, Pathophysiology, Diagnosis And Management Of Diabetes Mellitus
University of Gondar, Ethopia *Corresponding Author: Habtamu Wondifraw Baynes Lecturer Clinical Chemistry University of Gondar, Gondar Amhara 196, Ethiopia Tel: +251910818289 E-mail: [email protected] Citation: Baynes HW (2015) Classification, Pathophysiology, Diagnosis and Management of Diabetes Mellitus. J Diabetes Metab 6:541. doi:10.4172/2155-6156.1000541 Copyright: © 2015 Baynes HW. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Diabetes & Metabolism Abstract Diabetes Mellitus (DM) is a metabolic disorder characterized by the presence of chronic hyperglycemia either immune-mediated (Type 1 diabetes), insulin resistance (Type 2), gestational or others (environment, genetic defects, infections, and certain drugs). According to International Diabetes Federation Report of 2011 an estimated 366 million people had DM, by 2030 this number is estimated to almost around 552 million. There are different approaches to diagnose diabetes among individuals, The 1997 ADA recommendations for diagnosis of DM focus on fasting Plasma Glucose (FPG), while WHO focuses on Oral Glucose Tolerance Test (OGTT). This is importance for regular follow-up of diabetic patients with the health care provider is of great significance in averting any long term complications. Keywords Diabetes mellitus; Epidemiology; Diagnosis; Glycemic management Abbreviations DM: Diabetes Mellitus; FPG: Fasting Plasma Glucose; GAD: Glutamic Acid Decarboxylase; GDM: Gestational Diabetes Mellitus; HDL-cholesterol: High Density Lipoprotein cholesterol; HLA: Human Leucoid Antigen; IDD Continue reading >>
On Type 1 Diabetes Mellitus Pathogenesis
Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, Aghia Sophia Childrens Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece Correspondence should be addressed to C Kanaka-Gantenbein: chriskan{at}med.uoa.gr Type 1 diabetes mellitus (T1DM) results from the autoimmune destruction of cells of the endocrine pancreas. Pathogenesis of T1DM is different from that of type 2 diabetes mellitus, where both insulin resistance and reduced secretion of insulin by the cells play a synergistic role. We will present genetic, environmental and immunologic factors that destroy cells of the endocrine pancreas and lead to insulin deficiency. The process of autoimmune destruction takes place in genetically susceptible individuals under the triggering effect of one or more environmental factors and usually progresses over a period of many months to years, during which period patients are asymptomatic and euglycemic, but positive for relevant autoantibodies. Symptomatic hyperglycemia and frank diabetes occur after a long latency period, which reflects the large percentage of cells that need to be destroyed before overt diabetes become evident. Type 1 diabetes mellitus (T1DM) represents only around 10% of the diabetes cases worldwide, but occurs with increasing incidence much earlier in life. T1DM results from the autoimmune destruction of cells of the endocrine pancreas. A small percentage of affected patients (<10%) are classified as type 1B, with no evidence of autoimmunity and the pathogenesis in these cases is considered idiopathic ( 1 , 2 ). The aim of this comprehensive review is to present updated information on the pathogenesis of T1DM. We will present genetic, environmental and immunologic factors ( Table 1 ) that Continue reading >>
On Type 1 Diabetes Mellitus Pathogenesis
Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, Aghia Sophia Childrens Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece Received 2017 Nov 15; Accepted 2017 Nov 30. This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License . Type 1 diabetes mellitus (T1DM) results from the autoimmune destruction of cells of the endocrine pancreas. Pathogenesis of T1DM is different from that of type 2 diabetes mellitus, where both insulin resistance and reduced secretion of insulin by the cells play a synergistic role. We will present genetic, environmental and immunologic factors that destroy cells of the endocrine pancreas and lead to insulin deficiency. The process of autoimmune destruction takes place in genetically susceptible individuals under the triggering effect of one or more environmental factors and usually progresses over a period of many months to years, during which period patients are asymptomatic and euglycemic, but positive for relevant autoantibodies. Symptomatic hyperglycemia and frank diabetes occur after a long latency period, which reflects the large percentage of cells that need to be destroyed before overt diabetes become evident. Keywords: type 1 diabetes, pathogenesis, genetics, autoimmunity, microbiota Type 1 diabetes mellitus (T1DM) represents only around 10% of the diabetes cases worldwide, but occurs with increasing incidence much earlier in life. T1DM results from the autoimmune destruction of cells of the endocrine pancreas. A small percentage of affected patients (<10%) are classified as type 1B, with no evidence of autoimmunity and the pathogenesis in these cases is considered idiopathic ( 1 , 2 ). The aim of this comprehensive review is Continue reading >>
Diabetes Mellitus Type 1
Diabetes mellitus type 1 (also known as type 1 diabetes) is a form of diabetes mellitus in which not enough insulin is produced.[4] This results in high blood sugar levels in the body.[1] The classical symptoms are frequent urination, increased thirst, increased hunger, and weight loss.[4] Additional symptoms may include blurry vision, feeling tired, and poor healing.[2] Symptoms typically develop over a short period of time.[1] The cause of type 1 diabetes is unknown.[4] However, it is believed to involve a combination of genetic and environmental factors.[1] Risk factors include having a family member with the condition.[5] The underlying mechanism involves an autoimmune destruction of the insulin-producing beta cells in the pancreas.[2] Diabetes is diagnosed by testing the level of sugar or A1C in the blood.[5][7] Type 1 diabetes can be distinguished from type 2 by testing for the presence of autoantibodies.[5] There is no known way to prevent type 1 diabetes.[4] Treatment with insulin is required for survival.[1] Insulin therapy is usually given by injection just under the skin but can also be delivered by an insulin pump.[9] A diabetic diet and exercise are an important part of management.[2] Untreated, diabetes can cause many complications.[4] Complications of relatively rapid onset include diabetic ketoacidosis and nonketotic hyperosmolar coma.[5] Long-term complications include heart disease, stroke, kidney failure, foot ulcers and damage to the eyes.[4] Furthermore, complications may arise from low blood sugar caused by excessive dosing of insulin.[5] Type 1 diabetes makes up an estimated 5–10% of all diabetes cases.[8] The number of people affected globally is unknown, although it is estimated that about 80,000 children develop the disease each year.[5] With Continue reading >>
- Women in India with Gestational Diabetes Mellitus Strategy (WINGS): Methodology and development of model of care for gestational diabetes mellitus (WINGS 4)
- Postprandial Blood Glucose Is a Stronger Predictor of Cardiovascular Events Than Fasting Blood Glucose in Type 2 Diabetes Mellitus, Particularly in Women: Lessons from the San Luigi Gonzaga Diabetes Study
- Metabolic surgery for treating type 2 diabetes mellitus: Now supported by the world's leading diabetes organizations
Key Mechanism Involved In Type 2 Diabetes Identified
Follow all of ScienceDaily's latest research news and top science headlines ! Key mechanism involved in Type 2 diabetes identified Scientists have discovered a key protein that regulates insulin resistance -- the diminished ability of cells to respond to the action of insulin and which sets the stage for the development of the most common form of diabetes. This breakthrough points to a new way to potentially treat or forestall Type 2 diabetes, a rapidly growing global health problem. Scientists at the Gladstone Institutes have discovered a key protein that regulates insulin resistance -- the diminished ability of cells to respond to the action of insulin and which sets the stage for the development of the most common form of diabetes. This breakthrough points to a new way to potentially treat or forestall type 2 diabetes, a rapidly growing global health problem. In a paper being published online this week in the Proceedings of the National Academy of Sciences, researchers in the laboratory of Gladstone Investigator Katerina Akassoglou, PhD, describe an unexpected role of the p75 neurotrophin receptor in controlling how the body processes sugar. Called p75NTR, this receptor protein is usually associated with functions in neurons. "We identified that p75NTR is a unique player in glucose metabolism," said Dr. Akassoglou, who is also an associate professor of neurology at the University of California, San Francisco, with which Gladstone is affiliated. "Therapies targeted at p75NTR may represent a new therapeutic approach for diabetes." The pancreas makes a hormone called insulin that processes glucose, moving it from the bloodstream into the body's cells where it is used for energy. Insulin resistance is a key feature of Type 2 diabetes, in which glucose builds up in the b Continue reading >>
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Advances In The Etiology And Mechanisms Of Type 1 Diabetes
Specialty: Endocrinology, Immunology Institution: Diabetes Research Institute, Department of Medicine Division of Diabetes, Endocrinology and Metabolism, and Department of Microbiology and Immunology, University of Miami Miller School of Medicine Address: Miami, Florida, 33136, United States Abstract: Type 1 diabetes (T1D) is an insulin-dependent form of diabetes resulting from the autoimmune destruction of pancreatic beta cells. The past few decades have seen tremendous progress in our understanding of the molecular basis of the disease, with the identification of susceptibility genes and autoantigens, the demonstration of several abnormalities affecting various cell types and functions, and the development of improved assays to detect and monitor autoimmunity and beta cell function. New findings about the disease pathology and pathogenesis are emerging from extensive studies of organ donors with T1D promoted by the JDRF nPOD (Network for the Pancreatic Organ Donor with Diabetes). Furthermore, the establishment of extensive collaborative projects including longitudinal follow-up studies in relatives and clinical trials are setting the stage for a greater understanding of the role of environmental factors, the natural history of the disease, and the discovery of novel biomarkers for improved prediction, which will positively impact future clinical trials. Recent studies have highlighted the chronicity of islet autoimmunity and the persistence of some beta cell function for years after diagnosis, which could be exploited to expand therapeutic options and the time window during which a clinical benefit can be achieved. T1D is a multifactorial disease in which a genetic predisposition and environmental factors promote chronic autoimmunity against pancreatic beta cells. Ove Continue reading >>
