Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.
Curr Opin Endocrinol Diabetes Obes. 2012 Apr;19(2):81-7. doi: 10.1097/MED.0b013e3283514e13.
The association between obesity and insulin resistance is an area of much interest and enormous public health impact, with hundreds of articles being published in the last year focused on the possible mechanisms that underlie this association. The purpose to this review is to highlight some of the key recent literature with emphasis on emerging concepts.
The specific link between visceral adipose tissue accumulation and insulin resistance continues to be discerned. Visceral adiposity is correlated with accumulation of excess lipid in liver, and results in cell autonomous impairment in insulin signaling. Visceral adipose tissue is also prone to inflammation and inflammatory cytokine production, which also contribute to impairment in insulin signaling. The expansion of visceral adipose tissue and excess lipid accumulation in liver and muscle may result from limited expandability of subcutaneous adipose tissue, due to the properties of its extracellular matrix and capacity for capillary growth.
Recent studies underscore the need to better understand the mechanisms linking visceral adiposity with liver fat accumulation, the mechanisms by which ectopic fat accumulation cause insulin resistance, and the mechanisms by which the size of adipose tissue depots is determined.
肥胖与胰岛素抵抗之间的关联是一个备受关注且具有巨大公共卫生影响的领域，仅在过去一年中，就有数百篇文章聚焦于这一关联背后的可能机制。本文的目的是重点介绍一些关键的最新文献，并强调一些新出现的概念。
内脏脂肪组织堆积与胰岛素抵抗之间的具体联系仍在不断被揭示。内脏肥胖与肝脏中多余脂质的积累有关，导致细胞内胰岛素信号的自主损伤。内脏脂肪组织也容易发生炎症和炎性细胞因子的产生，这也会导致胰岛素信号的损伤。由于其细胞外基质的特性和毛细血管生长能力，皮下脂肪组织的扩展性有限，可能导致内脏脂肪组织的扩张和肝脏及肌肉中多余脂质的积累。
最近的研究强调需要更好地理解将内脏肥胖与肝脏脂肪积累联系起来的机制，了解异位脂肪积累导致胰岛素抵抗的机制，以及确定脂肪组织储量大小的机制。
