[1]郭绍东.组织特异性胰岛素抵抗及其代谢综合征的机制探讨[J].第三军医大学学报,2014,36(15):1535-1542.
 Guo Shaodong.Tissue-specific insulin resistance and its associated mechanisms for metabolic syndrome[J].J Third Mil Med Univ,2014,36(15):1535-1542.
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
36卷
期数:
2014年第15期
页码:
1535-1542
栏目:
专家述评
出版日期:
2014-08-15

文章信息/Info

Title:
Tissue-specific insulin resistance and its associated mechanisms for metabolic syndrome
作者:
郭绍东
Division of Molecular Cardiology,Department of Medicine,College of Medicine,Texas A&M University Health Science Center  1901 South 1st Street, Bldg. 205 Temple, TX 76504, USA
Author(s):
Guo Shaodong
Division of Molecular Cardiology, Department of Medicine, College of Medicine, Texas A&M University Health Science Center, TX 76504, USA
关键词:
胰岛素抵抗代谢综合征胰岛素受体底物12核转录因子FOXO1
Keywords:
insulin resistance metabolic syndrome insulin receptor substrate-12 forkhead transcription factor FOXO1
分类号:
R442.8;R587
文献标志码:
A
Abstract:
Metabolic syndrome, known as insulin resistance syndrome, has become a major public health problem worldwide. It is represented by a group of interrelated disorders, including obesity, hyperglycemia, hyperinsulinemia, hyperlipidemia, and hypertension. Metabolic syndrome is a high-risk factor for type 2 diabetes mellitus and cardiovascular diseases. As the most important hormone in the body in control of energy homeostasis, insulin and its signaling cascade normally control cell growth, metabolism and survival through activation of mitogen-activated protein kinases (MAPK) and phosphotidylinositide-3-kinase (PI3K), of which activation of PI-3K-associated with insulin receptor substrate 1 and 2 (IRS1, 2) and subsequent Akt→Foxo1 phosphorylation cascade, which has a central role in control of nutrient homeostasis and organ survival. Inactivation of Akt and activation of Foxo1, through suppressing IRS1 and IRS2 in different organs following hyperinsulinemia, metabolic inflammation, and over nutrition, may provide the underlying mechanisms for metabolic syndrome. Targeting the IRS→Akt→Foxo1 signaling cascade will likely provide a strategy for therapeutic intervention in the treatment of type 2 diabetes and its complications in humans. This review discussed how a deficiency of insulin signaling components in different organs contributes to the feature of the metabolic syndrome. Emphasis will be placed on the roles of IRS1, IRS2, and associated signaling pathways that couple to Akt and the forkhead/winged helix transcription factor FOXO1.

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更新日期/Last Update: 2014-07-25