Pathophysiology of insulin resistance
Pathophysiology of insulin resistance
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DOI：
10.1016/j.beem.2006.09.007
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发表时间：
2006-12-01
影响因子：
7.4
通讯作者：
Sesti, Giorgio
中科院分区：
文献类型：
--
作者：
Sesti, Giorgio
胰岛素抵抗是许多临床疾病的特征，包括2型糖尿病/葡萄糖耐受不良、肥胖、血脂异常和高血压聚集在所谓的代谢综合征中。骨骼肌的胰岛素抵抗主要表现为胰岛素刺激的糖原合成由于葡萄糖运输减少而减少。异位脂质积累在诱导胰岛素抵抗中起重要作用。胰岛素信号的多重缺陷是胰岛素抵抗受试者靶组织中糖代谢受损的原因。炎症分子和脂质代谢产物通过刺激一些不同的丝氨酸激酶来抑制胰岛素信号传导，这些丝氨酸激酶负责胰岛素受体底物- i （IRS-I）的丝氨酸磷酸化。
Insulin resistance is a feature of a number of clinical disorders, including type 2 diabetes/glucose intolerance, obesity, dyslipidaemia and hypertension clustering in the so-called metabolic syndrome. Insulin resistance in skeletal muscle manifests itself primarily as a reduction in insulin-stimulated glycogen synthesis due to reduced glucose transport. Ectopic lipid accumulation plays an important role in inducing insulin resistance. Multiple defects in insulin signalling are responsible for impaired glucose metabolism in target tissues of subjects with features of insulin resistance. Inflammatory molecules and lipid metabolites inhibit insulin signalling by stimulating a number of different serine kinases which are responsible for serine phosphorylation of Insulin Receptor Substrate-I (IRS-I).