Islet adaptation to insulin resistance: mechanisms and implications for intervention.
作者： B. Ahren , G. Pacini
DOI: 10.1111/J.1463-1326.2004.00361.X
关键词: Endocrinology 、 Insulin resistance 、 Hormone 、 Repaglinide 、 Metformin 、 Type 2 diabetes 、 Diabetes mellitus 、 Nateglinide 、 Medicine 、 Internal medicine 、 Insulin
摘要: Insulin sensitivity and insulin secretion are reciprocally related such that resistance is adapted by increased to maintain normal glucose lipid homeostasis. The relation between curvilinear mathematically best described as a hyperbolic relation. Several potential mediators have been suggested be signals for the beta cells respond glucose, free fatty acids, autonomic nerves, fat-derived hormones gut hormone glucagon-like peptide-1 (GLP-1). Failure of these or pancreatic adequately adapt in results inappropriate levels, impaired intolerance (IGT) type 2 diabetes. Therefore, treatment IGT diabetes should aim at restoring secretion. Such includes stimulation (sulphonylureas, repaglinide nateglinide) (metformin thiazolidinediones), well aimed supporting mediating islet adaptation (cholinergic agonists GLP-1). Both, correct understanding pathophysiology development novel modalities, therefore, non-linear inverse needs acknowledged.
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