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Diabetes mellitus is not one disease, but rather is a heterogeneous group of multifactorial, polygenic syndromes characterized by an elevation of fasting blood glucose that is caused by a relative or absolute deficiency in insulin.
The American Diabetes Association (ADA) recognizes four clinical classifications of diabetes: type 1 diabetes (formerly, insulin dependent diabetes mellitus), type 2 diabetes (formerly, non-insulin dependent diabetes mellitus), gestational diabetes, and diabetes due to other causes (for example, genetic defects or medications). Type 1 diabetics must rely on exogenous insulin injected subcutaneously to control hyperglycemia and ketoacidosis.
The goal in treating type 2 diabetes is to maintain blood glucose concentrations within normal limits, and to prevent the development of long-term complications. Gestational diabetes is defined as carbohydrate intolerance with onset or first recognition during pregnancy.
ReferenceInternational Diabetes Federation, Lippincott Illustrated Reviews Pharmacology & Biochemistry, American Diabetes Association, National Diabetes Education Program USA, Mayo Clinic.
Thankfulness to my father who shared with me regarding this web site, this website is in fact remarkable. We examined the restoration of first-phase and total insulin response as well as hepatic and peripheral insulin sensitivity. For example, it is estimated that more than 250 million people worldwide are afflicted with diabetes, and the prevalence is expected to exceed 350 million by the year 2030. Diabetes is the leading cause of adult blindness and amputation, and a major cause of renal failure, nerve damage, heart attacks, and stroke. The disease is characterized by an absolute deficiency of insulin caused by an autoimmune attack on the ? cells of the pancreas.
The goal in administering insulin to Type 1 diabetics is to maintain blood glucose concentrations as close to normal as possible and to avoid wide swings in glucose levels that may contribute to long-term complications. Insulin may also be delivered by a pump, which allows continuous subcutaneous infusion of insulin 24 hours a day at preset levels and the ability to program doses (a bolus) of insulin as needed at meal times. Weight reduction, exercise, and medical nutrition therapy (dietary modifications) often correct the hyperglycemia of newly diagnosed type 2 diabetes.
It is important to maintain adequate glycemic control during pregnancy, because uncontrolled gestational diabetes can lead to fetal macrosomia (abnormally large body) and shoulder dystocia (difficult delivery), as well as neonatal hypoglycemia.
A team of inspired pharmacists is working to build a free access pharma publication, we call it Pharma Mirror. Pharma Mirror has an International Standard Serial Number ISSN 2219-763X of its own and it has been assigned by ISSN Center, Paris. Additionally, to examine the mechanistic basis of observed outcomes, we quantified the change in fat content of the pancreas and liver The data are consistent with the hypothesis that the abnormalities of insulin secretion and insulin resistance that underlie type 2 diabetes have a single, common aetiology, i.e.


Insulin resistance is the decreased ability of target tissues, such as liver, adipose tissue, and muscle, to respond properly to normal (or elevated) circulating concentrations of insulin. In the absence of a defect in ?-cell function, non -diabetic, obese individuals can compensate for insulin resistance with elevated levels of insulin.
Hypoglycemic agents or insulin therapy may be required to achieve satisfactory plasma glucose levels. The metabolic abnormalities of type 1 diabetes mellitus include hyperglycemia, ketoacidosis, and hyper triacylglycerolemia. They result from a deficiency of insulin and a relative excess of glucagon. Glyburide and metformin may be reasonably safe alternatives to insulin therapy for gestational diabetes.
EnjoyIf you enjoyed this post, please consider subscribing to the RSS feed to have future articles delivered to your email inbox or feed reader. This provides a unified hypothesis to explain a common disease that previously appeared to require separate disease processes affecting the pancreas and insulin-sensitive tissues.
Rather, type 2 diabetes develops in insulin-resistant individuals who also show impaired ?-cell function. However, larger randomized studies are needed to fully assess neonatal outcomes and optimal dosing regimens. The metabolic alterations observed in type 2 diabetes are milder than those described for the insulin-dependent form of the disease, in part, because insulin secretion in type 2 diabetes- although not adequate- does restrain ketogenesis and blunts the development of diabetic ketoacidosis.
Prior to the onset of spontaneous diabetes in rodents, both total pancreatic fat and islet triacylglycerol content increase sharply. Available treatments for diabetes moderate the hyperglycemia, but fail to completely normalize metabolism.
In vitro, chronic saturated fatty acid exposure of beta cells inhibits the acute insulin response to glucose, and removal of fatty acids allows recovery of this response. The long standing elevation of blood glucose is associated with the chronic complications of diabetes- premature atherosclerosis, retinopathy, nephropathy, and neuropathy. The present data provide clear evidence that decreasing total pancreatic fat is associated with a return of beta cell function.
However, it is probable that the negative effect on beta cell function is exerted by toxic intermediaries such as diacylglycerol and ceramides, which change rapidly in response to acute metabolic changes, rather than by stored triacylglycerol per se, which acts as an index of fatty acid intermediary concentration.
Endless access to abundant calories from carbohydrate may be an evolutionarily novel, and thus pathology-inducing, situation.


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