神经酰胺
胰岛素抵抗
血脂异常
脂质代谢
生物
内分泌学
内科学
脂肪组织
2型糖尿病
糖尿病
医学
生物化学
细胞凋亡
作者
Hanin Aburasayn,Rami Al Batran,John R. Ussher
出处
期刊:American Journal of Physiology-endocrinology and Metabolism
[American Physiological Society]
日期:2016-08-01
卷期号:311 (2): E423-E435
被引量:77
标识
DOI:10.1152/ajpendo.00133.2016
摘要
Obesity is a major health concern that increases the risk for insulin resistance, type 2 diabetes (T2D), and cardiovascular disease. Thus, an enormous research effort has been invested into understanding how obesity-associated dyslipidemia and obesity-induced alterations in lipid metabolism increase the risk for these diseases. Accordingly, it has been proposed that the accumulation of lipid metabolites in organs such as the liver, skeletal muscle, and heart is critical to these obesity-induced pathologies. Ceramide is one such lipid metabolite that accumulates in tissues in response to obesity, and both pharmacological and genetic strategies that reduce tissue ceramide levels yield salutary actions on overall metabolic health. We will review herein why ceramide accumulates in tissues during obesity and how an increase in intracellular ceramide impacts cellular signaling and function as well as potential mechanisms by which reducing intracellular ceramide levels improves insulin resistance, T2D, atherosclerosis, and heart failure. Because a reduction in skeletal muscle ceramide levels is frequently associated with improvements in insulin sensitivity in humans, the beneficial findings reported for reducing ceramides in preclinical studies may have clinical application in humans. Therefore, modulating ceramide metabolism may be a novel, exciting target for preventing and/or treating obesity-related diseases.
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