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Mechanism Of Hyperglycemia In Diabetes

Investigating The Mechanism Of Hyperglycemia-induced Fetal Cardiac Hypertrophy

Investigating The Mechanism Of Hyperglycemia-induced Fetal Cardiac Hypertrophy

Investigating the Mechanism of Hyperglycemia-Induced Fetal Cardiac Hypertrophy Contributed equally to this work with: Sha-sha Han, Guang Wang, Ya Jin Affiliation Department of Pediatrics and Neonatology, Institute of Fetal-Preterm Labor Medicine, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China Contributed equally to this work with: Sha-sha Han, Guang Wang, Ya Jin Affiliation Division of Histology & Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou, 510632, China Contributed equally to this work with: Sha-sha Han, Guang Wang, Ya Jin Affiliation Department of Pediatrics and Neonatology, Institute of Fetal-Preterm Labor Medicine, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China Affiliation Division of Histology & Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou, 510632, China Affiliation Department of Pediatrics and Neonatology, Institute of Fetal-Preterm Labor Medicine, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China Affiliation Department of Pediatrics and Neonatology, Institute of Fetal-Preterm Labor Medicine, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China Affiliation Division of Histology & Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College, Jinan University, Guangzhou, 510632, China Affiliation Department of Pediatrics and Neonatology, Institute of Fetal-Preterm Labor Medicine, The First Affiliated Hospital, Jinan University, Guangzhou, 510630, China Affiliation Division of Histology & Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Educati Continue reading >>

Mechanisms For Hyperglycemia In Type Ii Diabetes Mellitus: Therapeuticimplications For Sulfonylurea Treatment--an Update.

Mechanisms For Hyperglycemia In Type Ii Diabetes Mellitus: Therapeuticimplications For Sulfonylurea Treatment--an Update.

Mechanisms for hyperglycemia in type II diabetes mellitus: therapeuticimplications for sulfonylurea treatment--an update. (1)Department of Medicine, University of Washington School of Medicine, Seattle. Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by fastinghyperglycemia associated with defects in the pancreatic islet, the liver, and theperipheral tissues, which together comprise a feedback loop responsible formaintenance of glucose homeostasis. This review focuses on the key role of theendocrine pancreas alpha and beta cells to coordinate glucose output from theliver with glucose utilization. The basal rate of hepatic glucose utilization.The basal rate of hepatic glucose production is elevated in subjects with NIDDM, and this is positively correlated with the degree of fasting hyperglycemia. This increased rate of glucose release by the liver results from impaired hepaticsensitivity to insulin, reduced insulin secretion, and increased glucagonsecretion. Though basal immunoreactive insulin levels in patients with NIDDM may appear normal when compared with healthy individuals, islet function testing atmatched glucose levels reveals impairments of basal, steady-state, and stimulatedinsulin secretion due to a reduction in beta-cell secretory capacity and areduced ability of glucose to suppress glucagon. The degree of impaired beta-cellresponsiveness to glucose is closely related to the degree of fastinghyperglycemia but in a curvilinear fashion. The efficiency of glucose uptake bythe peripheral tissues is also impaired due to a combination of decreased insulinsecretion and defective cellular insulin action. This impairment becomes moreimportant to the hyperglycemia as the islet alpha- and beta-cell functiondeclines. Therapeutic interventions, to be eff Continue reading >>

Hyperglycemia: New Mechanism Underlying Cardiovascular Disease Described

Hyperglycemia: New Mechanism Underlying Cardiovascular Disease Described

Follow all of ScienceDaily's latest research news and top science headlines ! Hyperglycemia: New mechanism underlying cardiovascular disease described Hyperglycemia starts a complex chain of events that damages blood vessels and cause cardiovascular disease. Scientists have now been able to demonstrate why this happens, as well as how the destructive chain can be broken. This discovery represents a crucial step towards an efficient treatment of the vascular injuries that will be the cause of death for most diabetes patients. Hyperglycemia starts a complex chain of events that damages blood vessels and cause cardiovascular disease. Scientists at Lund University Diabetes Centre (LUDC) have now been able to demonstrate why this happens, as well as how the destructive chain can be broken. This discovery represents a crucial step towards an efficient treatment of the vascular injuries that will be the cause of death for most diabetes patients. "This is a previously unexplored track that can explain how high blood sugar levels damage the blood vessels," says Maria Gomez, scientist at LUDC and the responsible author of the article, which is published online in the journal Arteriosclerosis, Thrombosis and Vascular Biology. At the end of the chain is the protein osteopontin. "Osteopontin is the black sheep of vascular biology. We know that elevated levels of this protein set off a cascade of inflammatory events that injures the blood vessel walls," says Maria Gomez. It is already known that diabetics have elevated levels of osteopontin in their blood and that there is a strong connection with diabetes complications. Inflammation is a basic mechanism underlying atherosclerotic plaque formation, which causes cardiac infarction and stroke. These diseases are the cause of death of Continue reading >>

How Hyperglycemia Promotes Atherosclerosis: Molecular Mechanisms

How Hyperglycemia Promotes Atherosclerosis: Molecular Mechanisms

Abstract Both type I and type II diabetes are powerful and independent risk factors for coronary artery disease (CAD), stroke, and peripheral arterial disease. Atherosclerosis accounts for virtually 80% of all deaths among diabetic patients. Prolonged exposure to hyperglycemia is now recognized a major factor in the pathogenesis of atherosclerosis in diabetes. Hyperglycemia induces a large number of alterations at the cellular level of vascular tissue that potentially accelerate the atherosclerotic process. Animal and human studies have elucidated three major mechanisms that encompass most of the pathological alterations observed in the diabetic vasculature: 1) Nonenzymatic glycosylation of proteins and lipids which can interfere with their normal function by disrupting molecular conformation, alter enzymatic activity, reduce degradative capacity, and interfere with receptor recognition. In addition, glycosylated proteins interact with a specific receptor present on all cells relevant to the atherosclerotic process, including monocyte-derived macrophages, endothelial cells, and smooth muscle cells. The interaction of glycosylated proteins with their receptor results in the induction of oxidative stress and proinflammatory responses 2) oxidative stress 3) protein kinase C (PKC) activation with subsequent alteration in growth factor expression. Importantly, these mechanisms may be interrelated. For example, hyperglycemia-induced oxidative stress promotes both the formation of advanced glycosylation end products and PKC activation. Advanced glycosylation end products The effects of hyperglycemia are often irreversible and lead to progressive cell dysfunction [8]. For example, in diabetic patients with functioning pancreatic transplants renal pathology continues to progress Continue reading >>

Mechanisms For Hyperglycemia In Type Ii Diabetes Mellitus: Therapeutic Implications For Sulfonylurea Treatmentan Update

Mechanisms For Hyperglycemia In Type Ii Diabetes Mellitus: Therapeutic Implications For Sulfonylurea Treatmentan Update

Volume 90, Issue 6, Supplement 1 , 24 June 1991, Pages S8-S14 Mechanisms for hyperglycemia in type II diabetes mellitus: Therapeutic implications for sulfonylurea treatmentan update Author links open overlay panel DanielPorteJrM.D. Get rights and content Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by fasting hyperglycemia associated with defects in the pancreatic islet, the liver, and the peripheral tissues, which together comprise a feedback loop responsible for maintenance of glucose homeostasis. This review focuses on the key role of the endocrine pancreas and cells to coordinate glucose output from the liver with glucose utilization. The basal rate of hepatic glucose production is elevated in subjects with NIDDM, and this is positively correlated with the degree of fasting hyperglycemia. This increased rate of glucose release by the liver results from impaired hepatic sensitivity to insulin, reduced insulin secretion, and increased glucagon secretion. Though basal immunoreactive insulin levels in patients with NIDDM may appear normal when compared with healthy individuals, islet function testing at matched glucose levels reveals impairments of basal, steady-state, and stimulated insulin secretion due to a reduction in -cell secretory capacity and a reduced ability of glucose to suppress glucagon. The degree of impaired -cell responsiveness to glucose is closely related to the degree of fasting hyperglycemia but in a curvilinear fashion. The efficiency of glucose uptake by the peripheral tissues is also impaired due to a combination of decreased insulin secretion and defective cellular insulin action. This impairment becomes more important to the hyperglycemia as the islet - and -cell function declines. Therapeutic interventions, to be effective Continue reading >>

Type 2 Diabetes Mellitus

Type 2 Diabetes Mellitus

Author: Romesh Khardori, MD, PhD, FACP; Chief Editor: George T Griffing, MD more... Type 2 diabetes mellitus consists of an array of dysfunctions characterized by hyperglycemia and resulting from the combination of resistance to insulin action, inadequate insulin secretion, and excessive or inappropriate glucagon secretion. See the image below. Simplified scheme for the pathophysiology of type 2 diabetes mellitus. See Clinical Findings in Diabetes Mellitus , a Critical Images slideshow, to help identify various cutaneous, ophthalmologic, vascular, and neurologic manifestations of DM. Many patients with type 2 diabetes are asymptomatic. Clinical manifestations include the following: Classic symptoms: Polyuria, polydipsia, polyphagia, and weight loss Diagnostic criteria by the American Diabetes Association (ADA) include the following [ 1 ] : A fasting plasma glucose (FPG) level of 126 mg/dL (7.0 mmol/L) or higher, or A 2-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or higher during a 75-g oral glucose tolerance test (OGTT), or A random plasma glucose of 200 mg/dL (11.1 mmol/L) or higher in a patient with classic symptoms of hyperglycemia or hyperglycemic crisis Whether a hemoglobin A1c (HbA1c) level of 6.5% or higher should be a primary diagnostic criterion or an optional criterion remains a point of controversy. Indications for diabetes screening in asymptomatic adults includes the following [ 2 , 3 ] : Overweight and 1 or more other risk factors for diabetes (eg, first-degree relative with diabetes, BP >140/90 mm Hg, and HDL < 35 mg/dL and/or triglyceride level >250 mg/dL) ADA recommends screening at age 45 years in the absence of the above criteria Microvascular (ie, eye and kidney disease) risk reduction through control of glycemia and blood pressure Macrovas Continue reading >>

Chronic Oxidative Stress As A Central Mechanism For Glucose Toxicity In Pancreatic Islet Beta Cells In Diabetes*

Chronic Oxidative Stress As A Central Mechanism For Glucose Toxicity In Pancreatic Islet Beta Cells In Diabetes*

Glucose in chronic excess causes toxic effects on structure and function of organs, including the pancreatic islet. Multiple biochemical pathways and mechanisms of action for glucose toxicity have been suggested. These include glucose autoxidation, protein kinase C activation, methylglyoxal formation and glycation, hexosamine metabolism, sorbitol formation, and oxidative phosphorylation. There are many potential mechanisms whereby excess glucose metabolites traveling along these pathways might cause beta cell damage. However, all these pathways have in common the formation of reactive oxygen species that, in excess and over time, cause chronic oxidative stress, which in turn causes defective insulin gene expression and insulin secretion as well as increased apoptosis. This minireview provides an overview of these mechanisms, as well as a consideration of whether antioxidant strategies might be used to protect further deterioration of the beta cell after the onset of diabetes and hyperglycemia. Diabetes mellitus is a disease characterized by hyperglycemia and is caused by absolute or relative insulin deficiency, sometimes associated with insulin resistance. It has multiple etiologies and segregates into two major forms. Type 1 diabetes is an autoimmune disease in which the patient's own immune system reacts against islet antigens and destroys the beta cell. Type 2 diabetes is a polygenic syndrome with multiple etiologies rather than a single specific disease. As the hyperglycemia of diabetes becomes chronic, the sugar that normally serves as substrate, fuel, and signal takes on the darker role of toxin. Chronic hyperglycemia is the proximate cause of retinopathy, kidney failure, neuropathies, and macrovascular disease in diabetes. The beta cell in type 2 diabetes is als Continue reading >>

Hyperglycemia

Hyperglycemia

Not to be confused with the opposite disorder, hypoglycemia. Hyperglycemia, or high blood sugar (also spelled hyperglycaemia or hyperglycæmia) is a condition in which an excessive amount of glucose circulates in the blood plasma. This is generally a blood sugar level higher than 11.1 mmol/l (200 mg/dl), but symptoms may not start to become noticeable until even higher values such as 15–20 mmol/l (~250–300 mg/dl). A subject with a consistent range between ~5.6 and ~7 mmol/l (100–126 mg/dl) (American Diabetes Association guidelines) is considered slightly hyperglycemic, while above 7 mmol/l (126 mg/dl) is generally held to have diabetes. For diabetics, glucose levels that are considered to be too hyperglycemic can vary from person to person, mainly due to the person's renal threshold of glucose and overall glucose tolerance. On average however, chronic levels above 10–12 mmol/L (180–216 mg/dL) can produce noticeable organ damage over time. Signs and symptoms[edit] The degree of hyperglycemia can change over time depending on the metabolic cause, for example, impaired glucose tolerance or fasting glucose, and it can depend on treatment.[1] Temporary hyperglycemia is often benign and asymptomatic. Blood glucose levels can rise well above normal and cause pathological and functional changes for significant periods without producing any permanent effects or symptoms. [1] During this asymptomatic period, an abnormality in carbohydrate metabolism can occur which can be tested by measuring plasma glucose. [1] However, chronic hyperglycemia at above normal levels can produce a very wide variety of serious complications over a period of years, including kidney damage, neurological damage, cardiovascular damage, damage to the retina or damage to feet and legs. Diabetic n Continue reading >>

Mechanisms For Hyperglycemia In Type Ii Diabetes Mellitus: Therapeutic Implications For Sulfonylurea Treatmentan Update

Mechanisms For Hyperglycemia In Type Ii Diabetes Mellitus: Therapeutic Implications For Sulfonylurea Treatmentan Update

Volume 90, Issue 6, Supplement 1 , 24 June 1991, Pages S8-S14 Mechanisms for hyperglycemia in type II diabetes mellitus: Therapeutic implications for sulfonylurea treatmentan update Author links open overlay panel DanielPorteJrM.D. Get rights and content Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by fasting hyperglycemia associated with defects in the pancreatic islet, the liver, and the peripheral tissues, which together comprise a feedback loop responsible for maintenance of glucose homeostasis. This review focuses on the key role of the endocrine pancreas and cells to coordinate glucose output from the liver with glucose utilization. The basal rate of hepatic glucose production is elevated in subjects with NIDDM, and this is positively correlated with the degree of fasting hyperglycemia. This increased rate of glucose release by the liver results from impaired hepatic sensitivity to insulin, reduced insulin secretion, and increased glucagon secretion. Though basal immunoreactive insulin levels in patients with NIDDM may appear normal when compared with healthy individuals, islet function testing at matched glucose levels reveals impairments of basal, steady-state, and stimulated insulin secretion due to a reduction in -cell secretory capacity and a reduced ability of glucose to suppress glucagon. The degree of impaired -cell responsiveness to glucose is closely related to the degree of fasting hyperglycemia but in a curvilinear fashion. The efficiency of glucose uptake by the peripheral tissues is also impaired due to a combination of decreased insulin secretion and defective cellular insulin action. This impairment becomes more important to the hyperglycemia as the islet - and -cell function declines. Therapeutic interventions, to be effective Continue reading >>

Pathogenesis Of Chronic Hyperglycemia: From Reductive Stress To Oxidative Stress

Pathogenesis Of Chronic Hyperglycemia: From Reductive Stress To Oxidative Stress

Pathogenesis of Chronic Hyperglycemia: From Reductive Stress to Oxidative Stress Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, RES-314E, Fort Worth, TX 76107, USA Received 29 April 2014; Accepted 27 May 2014; Published 16 June 2014 Academic Editor: KonstantinosPapatheodorou Copyright 2014 Liang-Jun Yan. 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. Chronic overnutrition creates chronic hyperglycemia that can gradually induce insulin resistance and insulin secretion impairment. These disorders, if not intervened, will eventually be followed by appearance of frank diabetes. The mechanisms of this chronic pathogenic process are complex but have been suggested to involve production of reactive oxygen species (ROS) and oxidative stress. In this review, I highlight evidence that reductive stress imposed by overflux of NADH through the mitochondrial electron transport chain is the source of oxidative stress, which is based on establishments that more NADH recycling by mitochondrial complex I leads to more electron leakage and thus more ROS production. The elevated levels of both NADH and ROS can inhibit and inactivate glyceraldehyde 3-phosphate dehydrogenase (GAPDH), respectively, resulting in blockage of the glycolytic pathway and accumulation of glycerol 3-phospate and its prior metabolites along the pathway. This accumulation then initiates all those alternative glucose metabolic pathways such as the polyol pathway and the advanced glycation pathways that otherwise are minor and insignificant under euglycem Continue reading >>

Diabetes: Mechanism, Pathophysiology And Management-a Review

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: prof.an[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 >>

The Pathogenesis And Pathophysiology Of Type 1 And Type 2 Diabetes Mellitus

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 >>

Obesity-induced Insulin Resistance And Hyperglycemia: Etiologic Factors And Molecular Mechanisms

Obesity-induced Insulin Resistance And Hyperglycemia: Etiologic Factors And Molecular Mechanisms

TYPE-2 diabetes is a polygenic disease. Obesity has been identified as a major causative factor for the insulin resistance and hyperglycemia associated with diabetes.1 Developed and developing countries alike are experiencing a sharp rise in the incidence of obesity-linked type-2 diabetes.2 Consequently, obesity-induced diabetes is emerging as a global health-care problem threatening to reach pandemic levels by 2030, when the incidence is projected to more than double in a period of only 30 years (from 171 million in 2000 to 366 million in 2030).3 The problem is not limited to adults. There has also been a marked increase in obesity (defined as a body mass index of greater than 30 kg/m2) among children.4 In the early stages of type-2 diabetes, insulin resistance is countered by a state of hyperinsulinemia brought about by stepped-up insulin production in the pancreas. Euglycemia is therefore maintained. Overt hyperglycemia does not develop until later stages, when pancreatic β cells can no longer compensate for the high levels of insulin resistance in peripheral tissues. Along with diabetes, there has been a concomitant increase of the incidence of metabolic syndrome, an obesity-linked condition characterized by clinical features of insulin resistance, dyslipidemia, and hypertension.5,6 Ultimately, it is the compounding effects of these cardiovascular, renal, cerebral, and thrombogenic anomalies that give rise to the increased morbidity and mortality associated with obesity, type-2 diabetes, and metabolic syndrome.6 Malfunctions in energy homeostasis resulting from genetic predisposition can lead to obesity. However, the recent increase in obesity is not thought to be due to specific congenital or hereditary defects in lipid metabolism, but to the inability of the body Continue reading >>

Pathogenesis Of Type 2 Diabetes Mellitus

Pathogenesis Of Type 2 Diabetes Mellitus

INTRODUCTION Type 2 diabetes mellitus is characterized by hyperglycemia, insulin resistance, and relative impairment in insulin secretion. It is a common disorder with a prevalence that rises markedly with increasing degrees of obesity (figure 1) [1]. The prevalence of type 2 diabetes has risen alarmingly in the past decade [2], in large part linked to the trends in obesity and sedentary lifestyle [3]. PATHOPHYSIOLOGY Understanding the pathogenesis of type 2 diabetes is complicated by several factors [4]. Patients present with a combination of varying degrees of insulin resistance and relative insulin deficiency, and it is likely that both contribute to type 2 diabetes [5-7]. Furthermore, each of the clinical features can arise through genetic or environmental influences, making it difficult to determine the exact cause in an individual patient. Moreover, hyperglycemia itself can impair pancreatic beta-cell function and exacerbate insulin resistance, leading to a vicious cycle of hyperglycemia causing a worsening metabolic state [8]. Type 2 diabetes is often accompanied by other conditions, including hypertension, high serum low-density lipoprotein (LDL) cholesterol concentrations, and low serum high-density lipoprotein (HDL) cholesterol concentrations that, like type 2 diabetes, increase cardiovascular risk. This constellation of clinical conditions is referred to as the metabolic syndrome [9]. Hyperinsulinemia occurring in response to insulin resistance may play an important role in the genesis of these abnormalities. Increased free fatty acid levels, inflammatory cytokines from fat, and oxidative factors have all been implicated in the pathogenesis of metabolic syndrome, type 2 diabetes, and their cardiovascular complications. (See "The metabolic syndrome (insulin re Continue reading >>

Classification, Pathophysiology, Diagnosis And Management Of Diabetes Mellitus

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 >>

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