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Mechanism Of Type 1 Diabetes Mellitus

Pathogenesis Of Type 2 Diabetes

Pathogenesis Of Type 2 Diabetes

Please confirm that you would like to log out of Medscape.If you log out, you will be required to enter your username and password the next time you visit. Log out Cancel Insulin resistance often is the primary metabolic abnormality leading to the development of type 2 diabetes. Type 2 diabetes can be viewed as the consequence of a series of pathophysiologic changes, each of which makes the patient vulnerable to subsequent disruption of normal glucose homeostasis. In most individuals, insulin resistance is the first of a sequence of abnormalities leading to the development of type 2 diabetes. Insulin resistance is compensated by increased insulin secretion (hyperinsulinemia), which allows glucose metabolism to remain normal. The beta cells in genetically susceptible individuals become impaired, leading to delayed and insufficient insulin secretion. Due to decreasing beta-cell function, the individual with insulin resistance first develops postprandial hyperglycemia and subsequently develops fasting hyperglycemia. Chronic hyperglycemia contributes to a further suppression of pancreatic beta-cell insulin secretion and worsens insulin resistance. These 3 components (insulin resistance, insulin deficiency, and glucose toxicity) are the targets of our therapeutic interventions. The distinction between insulin-sensitive and insulin-resistant type 2 diabetes is important when considering treatment. A drug that treats insulin resistance may be the drug of choice for an insulin-resistant patient, but should not be prescribed for a patient with insulin-sensitive diabetes. In the United States, nearly 30 million individuals have some form of glucose intolerance or diabetes (type 1 or, much more commonly, type 2).[ 1 ] Further breakdown of these numbers reveals critical facts for 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: [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 >>

Diabetes Mellitus Type 1

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 >>

Review Article Pathogenesis Of Type 2 Diabetes Mellitus

Review Article Pathogenesis Of Type 2 Diabetes Mellitus

The pathological sequence for type 2 diabetes is complex and entails many different elements that act in concert to cause that disease. This review proposes 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 factors that share an ability to stress the glucose homeostasis system, with the current explosion of obesity and sedentary lifestyle being a major cause of the worldwide diabetes epidemic. We also propose that a lowered beta-cell mass either through genetic 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 beta cell's glucose responsiveness to meals by impairing the first phase insulin response—and cause the blood glucose level to rise into the range of impaired glucose tolerance (IGT). This rise in blood glucose, now perhaps in concert with the excess fatty acids that are a typical feature of obesity and insulin resistance, cause additional deterioration in beta-cell function along with further insulin resistance, and the blood glucose levels rise to full-blown diabetes. This sequence also provides insight into how to better prevent or treat type 2 diabetes, by studying the molecular basis for the early defects, and developing targeted therapies against them. Continue reading >>

The Epidemiology, Pathogenesis, And Treatment Of Type 1 Diabetes Mellitus

The Epidemiology, Pathogenesis, And Treatment Of Type 1 Diabetes Mellitus

Abstract Type 1 diabetes mellitus (T1DM), also known as insulin-dependent diabetes, is a chronic disease caused by autoimmune (type 1a) or spontaneous (type 1b) destruction of pancreatic beta cells, resulting in insulin deficiency. It is generally diagnosed in children before 20 years of age and is oftentimes fatal. This review will discuss the epidemiology of T1DM, including its incidence and prevalence, related temporal trends and risk factors for development. Furthermore, pathogenesis and immune system involvement of the disease will be evaluated, with a particular focus on cells of the adaptive and innate immune systems. Finally, an overview of past, present and future treatments for T1DM will be discussed. Type 1 diabetes mellitus (T1DM), also known as insulin-dependent diabetes, is a chronic disease caused by autoimmune (type 1a) or spontaneous (type 1b) destruction of pancreatic beta cells, resulting in insulin deficiency (Haller, Atkinson & Schatz, 2005) (Kim & Lee, 2009). A lack of insulin causes hyperglycaemia (high blood glucose levels), resulting in recurrent urination (polyuria); augmented thirst (polydipsia) and hunger (polyphagia); and weight loss (Haller, Atkinson & Schatz, 2005) (Gan, Albanese-O’Neill & Haller, 2012). Accounting for 10% of total diabetes cases, T1DM affects millions of individuals worldwide (Kim & Lee, 2009) (Achenbach, Bonifacio & Ziegler, 2005). It is generally diagnosed in children before 20 years of age (Gan, Albanese-O’Neill & Haller, 2012) (Maahs, West, Lawrence et al., 2010). Furthermore, the Juvenile Diabetes Research Foundation International (JDRF Int.) predicts an increase in the incidence of the disease among youth in upcoming years (Kim & Lee, 2009). Unfortunately, T1DM is fatal without treatment (Gan, Albanese-O’Neill Continue reading >>

Type 1 Diabetes Mellitus

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 >>

Mechanisms In Endocrinology: Insulin And Type 1 Diabetes: Immune Connections

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 >>

Pathogenesis Of Type 1 Diabetes Mellitus

Pathogenesis Of Type 1 Diabetes Mellitus

INTRODUCTION Type 1A diabetes mellitus results from autoimmune destruction of the insulin-producing beta cells in the islets of Langerhans [1]. This process occurs in genetically susceptible subjects, is probably triggered by one or more environmental agents, and usually progresses over many months or years during which the subject is asymptomatic and euglycemic. Thus, genetic markers for type 1A diabetes are present from birth, immune markers are detectable after the onset of the autoimmune process, and metabolic markers can be detected with sensitive tests once enough beta cell damage has occurred, but before the onset of symptomatic hyperglycemia [2]. This long latent period is a reflection of the large number of functioning beta cells that must be lost before hyperglycemia occurs (figure 1). Type 1B diabetes mellitus refers to nonautoimmune islet destruction (Type 1B diabetes). (See "Classification of diabetes mellitus and genetic diabetic syndromes".) The pathogenesis of type 1A diabetes is quite different from that of type 2 diabetes mellitus, in which both decreased insulin release (not on an autoimmune basis) and insulin resistance play an important role. Genome-wide association studies indicate that type 1 and type 2 diabetes' genetic loci do not overlap, although inflammation (eg, interleukin-1 mediated) may play a role in islet beta cell loss in both types [3]. (See "Pathogenesis of type 2 diabetes mellitus".) The pathogenesis of type 1 diabetes mellitus will be reviewed here. The diagnosis and management of type 1 diabetes are discussed separately. (See "Epidemiology, presentation, and diagnosis of type 1 diabetes mellitus in children and adolescents" and "Prevention of type 1 diabetes mellitus" and "Management of type 1 diabetes mellitus in children and ado Continue reading >>

What Is Diabetes Mellitus?

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 >>

Type 1 Diabetes: Pathogenesis And Prevention

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 >>

Advances In The Etiology And Mechanisms Of Type 1 Diabetes

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 >>

Current Concepts On The Pathogenesis Of Type 1 Diabetes—considerations For Attempts To Prevent And Reverse The Disease

Current Concepts On The Pathogenesis Of Type 1 Diabetes—considerations For Attempts To Prevent And Reverse The Disease

Historical Model of Type 1 Diabetes Pathogenesis It may be considered unusual to consider a period of three decades “historical.” Yet, the evolution for our understanding of the natural history and pathogenesis of type 1 diabetes has been greatly advanced by a vast number of studies aimed at validating a model (1), proposed by the late Dr. George Eisenbarth in 1986 (2). As a result of this work, the majority of current conventional wisdom portrays type 1 diabetes as a T cell–mediated autoimmune disease involving the specific destruction of insulin-producing pancreatic β-cells. In this model, persons destined to develop type 1 diabetes are assumed to begin life with a full cadre of β-cells. However, a “triggering” insult, likely environmental, initiates a process involving the recruitment of antigen-presenting cells. Antigen-presenting cells sequester self-antigens released by injured β-cells, followed by their transport to pancreatic lymph nodes where they are subsequently presented to autoreactive T cells. These T cells, rogue constituents brought to life due to genetically driven failures of thymic deletion (i.e., central tolerance) combined with defects in mechanisms designed to induce peripheral immune tolerance, come into play (3). This toxic duo, imparting lack-of-tolerance formation, again in the context of genetic susceptibility, allows for migration of self-reactive T cells to islets, mediating β-cell killing and promoting further inflammation (4). When 85–90% of pancreatic β-cells meet their demise, symptoms of the disease occur. In the final stage of the model, the autoimmune process ends with the complete elimination of β-cells. While this concept still forms the prevailing intellectual dogma for the majority of individuals associated with Continue reading >>

On Type 1 Diabetes Mellitus Pathogenesis

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 >>

Aetiology And Pathogenesis Of Type 1 Diabetes Mellitus : Oxford Textbook Of Endocrinology And Diabetes

Aetiology And Pathogenesis Of Type 1 Diabetes Mellitus : Oxford Textbook Of Endocrinology And Diabetes

(p. 1712) Aetiology and pathogenesis of type 1 diabetes mellitus (p. 1712) Aetiology and pathogenesis of type 1 diabetes mellitus Oxford Textbook of Endocrinology and Diabetes (2 ed.) As described in Chapter 13.2.3, type 1 diabetes results from the destruction of the glucose-responsive, insulin-secreting cells of the pancreatic islets. Its principal clinical features reflect significant insulin deficiency. In general, the cell damage is immune mediated and other clinical features occur related to other autoimmune processes. Although typically considered to have a short prodrome, in research studies biochemical evidence of impaired glucose metabolism has been detected years before diagnosis, in the form of mild elevation of blood glucose. It is likely that the clinical symptoms only manifest when 90% or more of the cells are lost. The effects of insulin deficiency are enhanced at times of insulin resistance, which explains the apparent link between clinical onset of type 1 diabetes and acute stress, such as an intercurrent infection or other illness, or physiological changes in insulin resistance, such as during puberty. The rate of cell loss is highly variable. It is probable that type 1 diabetes presenting in prepubertal childhood may reflect a more aggressive destructive process, while, at the other extreme, type 1 diabetes may present in adult life with a slow evolution to an absolute need for insulin replacement. The latter is called latent adult onset diabetes (LADA), and confounds the clinical definition of type 1 diabetesoften used in recruiting type 1 patients to trialsof requirement for insulin replacement within a year of diagnosis. The diagnosis of type 1A diabetes, i.e. type 1 diabetes of proven autoimmune pathogenesis, may be made by finding evidence of th Continue reading >>

Pathogenesis - Type 1 Diabetes Mellitus - Diapedia, The Living Textbook Of Diabetes

Pathogenesis - Type 1 Diabetes Mellitus - Diapedia, The Living Textbook Of Diabetes

The metabolic consequences of type 1 diabetes result from progressive beta cell deficiency due to loss of functional beta cells. This section reviews the evidence that beta cell destruction is mediated by the immune system, and the associated histopathological changes in the pancreatic islets. The immunological mechanisms involved include humoral and cellular immune responses directed against beta cell constituents, with a further potential contribution from the innate immune system. Possible models of immune-mediated beta cell destruction are outlined, and the role of animal models of type 1 diabetes is described. The aetiology ('cause') of type 1 diabetes is unknown, but a good deal is known about its pathogenesis (the way in which it develops). As with other complex diseases, the outcome is determined by the interplay of multiple genes and (most likely) multiple environmental determinants, together with an element of happenstance. The risk of developing diabetes is strongly influenced by genes affecting immune function, particularly the HLA system, but other factors are involved. The best evidence for this comes from the study of identical twins: if one twin develops diabetes in childhood, the other (who has identical genes) has no more than a one in three chance of developing the disease. Prospective studies in human populations reveal that circulating autoantibodies directed against the islets typically appear in the first 5 years of life, and may be present for many years (sometimes 20 years or more) before the disease develops. A similar latent period is seen with coeliac disease, and implies that some sort of regulatory balance has been achieved within the immune system, and subsequently lost. This opens the door to the possibility of 're-education' of the immu Continue reading >>

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