Protein kinase C-beta: An emerging connection between nutrient excess and obesity.

Protein kinase C-beta: An emerging connection between nutrient excess and obesity.
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DOI:
10.1016/j.bbalip.2014.07.011
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发表时间:
2014-10
期刊:
Biochimica et biophysica acta
影响因子:
--
通讯作者:
Neil K Mehta;K. Mehta
Neil K Mehta;K. Mehta
中科院分区:
其他
文献类型:
--
作者:
Neil K Mehta;K. Mehta

文献摘要

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由于最近生活方式的改变,目前肥胖症在全球流行。过量的身体脂肪沉积是由于遗传和环境因素之间的相互作用引起的能量摄入和能量消耗之间的不平衡造成的。通过破坏能量稳态来触发脂肪积累的信号和生物学机制还没有很好地理解。现在有大量证据支持蛋白激酶C β(PKCβ)在能量稳态中的可能作用。本文综述了PKCβ激活在肥胖发生和发展中的作用以及PKCβ抑制在调节体育锻炼有益作用中的作用。现有数据支持一种模型,其中脂肪PKCβ激活是通过与p66shc相互作用破坏线粒体功能并放大脂肪蓄积和脂肪功能障碍的起始事件之一,具有全身性后果。PKCβ水平、活性或信号传导的操纵可以提供对抗肥胖和相关代谢紊乱的治疗方法。
There is currently a global epidemic of obesity as a result of recent changes in lifestyle. Excess body fat deposition is caused by an imbalance between energy intake and energy expenditure due to interactions between genetic and environmental factors. The signals and biological mechanisms that trigger fat accumulation by disrupting energy homeostasis are not well understood. There is considerable evidence now supporting a possible role of protein kinase C beta (PKCβ) in energy homeostasis. This review highlights recent findings on the role of PKCβ activation in the genesis and progression of obesity, and of PKCβ repression in mediating the beneficial effects of physical exercise. Available data support a model in which adipose PKCβ activation is among the initiating events that disrupt mitochondrial function through interaction with p66shcand amplify fat accumulation and adipose dysfunction, with systemic consequences. Manipulation of PKCβ levels, activity, or signaling could provide a therapeutic approach to combat obesity and associated metabolic disorders.