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脂肪感知与代谢综合征

Fat sensing and metabolic syndrome.

作者信息

Youn Jang H

机构信息

Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, CA, USA,

出版信息

Rev Endocr Metab Disord. 2014 Dec;15(4):263-75. doi: 10.1007/s11154-014-9300-1.

DOI:10.1007/s11154-014-9300-1
PMID:25344446
Abstract

Overconsumption of dietary fat contributes to the development of obesity and metabolic syndrome. Recent evidence suggests that high dietary fat may promote these metabolic states not only by providing calories but also by inducing impaired control of energy balance. In normal metabolic states, fat interacts with various organs or receptors to generate signals for the regulation of energy balance. Many of these interactions are impaired by high-fat diets or in obesity, contributing to the development or maintenance of obesity. These impairments may arise largely from fundamental alterations in the hypothalamus where all peripheral signals are integrated to regulate energy balance. This review focuses on various mechanisms by which fat is sensed at different stages of ingestion, circulation, storage, and utilization to regulate food intake, and how these individual mechanisms are altered by high-fat diets or in obesity.

摘要

膳食脂肪摄入过多会导致肥胖和代谢综合征的发生。最近的证据表明,高膳食脂肪可能不仅通过提供热量,还通过导致能量平衡控制受损来促进这些代谢状态。在正常代谢状态下,脂肪与各种器官或受体相互作用,产生调节能量平衡的信号。高脂肪饮食或肥胖会损害其中许多相互作用,从而导致肥胖的发生或维持。这些损害可能主要源于下丘脑的根本改变,所有外周信号在此整合以调节能量平衡。本综述重点关注在摄入、循环、储存和利用的不同阶段脂肪被感知以调节食物摄入的各种机制,以及这些个体机制在高脂肪饮食或肥胖状态下是如何改变的。

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本文引用的文献

1
Induced ablation of ghrelin cells in adult mice does not decrease food intake, body weight, or response to high-fat diet.成年小鼠中胃饥饿素细胞的诱导消融不会降低食物摄入量、体重或对高脂饮食的反应。
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