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|Type:||Capítulo de livro|
|Title:||Insulin Secretion In Insulin Resistance States|
De Barros-Mazon S.
|Abstract:||Insulin secretion is regulated mainly by glucose stimulus changes and is characterized by first and second phase (biphasic time course). β-cell glucose sensitivity is essential to maintain glucose homeostasis and loss of that capacity has been related to progression from normal glucose tolerance to impaired glucose tolerance and diabetes mellitus. β-cell glucose sensitivity can be evaluated through a slope of dose-response curve which shows the ability to increase insulin release with the appropriate amount and time course to cope with acute changes in plasma glucose concentration. Some factors can modulate insulin secretion. One of them is glucose toxicity, the direct impairment of chronic hyperglycemia on β-cell function characterized as impairment in insulin response to glucose but not to other nonglucose secretagogues. A glucose-induced insulin secretion is completely restored if normoglycemia is achieved. Lipotoxicity is also related to lower glucose induced insulin secretion through different mechanisms. On the other hand, it is suggested that the incretin GLP-1 stimulates insulin secretion through increasing β-cell glucose sensitivity, inhibiting potassium channels and exacerbating the voltage-dependent calcium channels. Normoglycemia in states of insulin resistance is maintained by a compensatory increase in insulin secretion. Adipokines such as pro-inflammatory cytokines are related to insulin resistance in obesity and type 2 diabetes. The mechanisms underlying regulated-insulin secretion by adipokines and insulin resistance are very complex and not completely understood. In fact a real molecular and cellular inflammatory network takes place acting per se linking up lipotoxicity, glucotoxicity and insulin secretion. Adiponectin and weight loss, on the other hand, are related to the decrease in the pro-inflammatory state and improved insulin action and secretion. So the focus of this review is to address the mechanisms underlying reciprocal relationships between insulin secretion, insulin resistance and inflammation in the pathological state and in its subsequent improvement. © 2010 by Nova Science Publishers, Inc. All rights reserved.|
|Editor:||Nova Science Publishers, Inc.|
|Appears in Collections:||Unicamp - Artigos e Outros Documentos|
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