Diabetul zaharat: O chemare la acţiune - ppt download
Over time, changes in insulin resistance and secretion lead to the onset of type 2 diabetes. In the early stages, as insulin resistance rises, there is a compensatory increase in insulin secretion and glucose levels remain normal normoglycemia.
In the long term, however, as the b-cells begin to fail, insulin secretion falls, IGT and hyperglycemia become apparent and frank type 2 diabetes develops. IGT may be defined as higher than normal blood glucose levels, but not high enough to be called diabetes.
People with IGT may or may not go on to develop diabetes. Glucose levels both before fasting and lemieux anti-imbatranire post-prandial meals increase steadily as the individual progresses from normoglycemia to IGT and, finally, type 2 diabetes. Citation: Holman RR. Assessing the potential for alpha-glucosidase inhibitors in prediabetic states.
Diabetes Res Clin Pract ;40 suppl :S Lebovitz H. Diabetes Rev ;— Holman RR. A remorseless progression of the lemieux anti-imbatranire endocrine defects of insulin resistance and b-cell dysfunction begins years before the diagnosis of type 2 diabetes and occurs throughout the evolution of dysglycaemia. Initially, insulin resistance causes the glucose-lowering actions of insulin to be blunted, so that the pancreas secretes more insulin to overcome the deficit.
At this stage the subject may develop impaired glucose tolerance, but is not yet diabetic.
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As insulin resistance progresses, the pancreas is no longer able to secrete enough insulin to control glycaemia, and increased hepatic glucose output and reduced glucose disposal by muscle and fat contribute to the chronic fasting and postprandial hyperglycaemia characteristic of type 2 diabetes. Diabetes Care ; DeFronzo R et al.
J Clin Invest. Professor Reaven called this entity "Syndrome X," but it is more commonly called the metabolic syndrome, or the insulin resistance syndrome.
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Note that Professor Reaven listed glucose intolerance rather than diabetes, since subjects who developed type 2 diabetes need a second deficit, which is lemieux anti-imbatranire insulin secretion. As a result, many or most individuals with insulin resistance will cum se aplică plasturi pe pliurile nazolabiale actually have type 2 diabetes. In his Banting lecture, Professor Reaven attempted to show that people can have the insulin resistance syndrome even without obesity.
However, other investigators such as Després have noted that insulin resistance occurs most often in combination with increases in visceral fat.
Not all of the components described in the Banting lecture are equally strongly related to insulin resistance.
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A number of techniques including factor analysis have been used to suggest that hypertension has no or only a very weak relationship to insulin resistance. References: Reaven GM. Banting lecture role of insulin resistance in human disease.
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Waist circumference and abdominal sagittal diameter: best simple anthropometric indexes of abdominal visceral adipose tissue accumulation and related cardiovascular risk in men and women. Metabolic and inflammation variable clusters and prediction of type 2 diabetes: factor analysis using directly measured insulin sensitivity.
These additional candidates have included small, dense LDL and a group of novel risk factors including elevated CRP levels, plasminogen activator inhibitor—1 PAI-1and fibrinogen.
Other investigators have noted that insulin resistance occurs in women with polycystic ovarian syndrome, and some authors are now making an association between insulin resistance and nonalcoholic fatty liver disease NAFLD.
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In a more recent review, Professor Reaven acknowledges the importance of visceral adiposity. Reference: Reaven G. Syndrome X: 10 years after. Drugs ;58 suppl 1 Drugs ;58 suppl with permission from WolthersKluwer Health. The IDF have now proposed a unified definition, in order to facilitate comparisons between studies, and the development of treatment strategies.