Adipokines mediate inflammation and insulin resistance.
Adipokines mediate inflammation and insulin resistance.
复制标题
DOI：
10.3389/fendo.2013.00071
复制
发表时间：
2013
影响因子：
5.2
通讯作者：
Pessin JE
中科院分区：
文献类型：
--
作者：
Kwon H;Pessin JE
多年来，脂肪组织被认为是一种惰性能量储存器官，它在能量过剩时积累和储存甘油三酯，在全身能量需要时释放脂肪酸。然而，在过去的二十年中，脂肪组织仓库已经被确立为高度活跃的内分泌和代谢重要器官，可以调节能量消耗和葡萄糖稳态。在啮齿类动物中，棕色脂肪组织在非寒战产热和能量消耗中起着至关重要的作用，可以防止饮食引起的肥胖。白色脂肪组织也被统称为皮下或内脏脂肪组织，负责一系列信号分子的分泌，称为脂肪因子。这些脂肪因子作为经典的循环激素发挥作用，与其他器官包括大脑、肝脏、肌肉、免疫系统和脂肪组织本身进行交流。脂肪因子的失调与肥胖、2型糖尿病和心血管疾病有关。近年来，脂肪组织的炎症反应已被证明是诱导外周组织胰岛素抵抗的主要机制。虽然瘦素和脂联素调节摄食行为和能量消耗，但这些脂肪因子也参与炎症反应的调节。脂肪组织分泌各种促炎性和抗炎性脂肪因子来调节炎症和胰岛素抵抗。在肥胖人和啮齿动物模型中，促炎脂肪因子的表达增强，诱导胰岛素抵抗。总的来说，这些发现表明，肥胖引起的胰岛素抵抗可能至少部分是由于促炎性和抗炎性脂肪因子表达的不平衡。本文就脂肪因子在肥胖引起的炎症和胰岛素抵抗中的生理和分子功能的研究进展进行综述，并对未来的研究方向进行展望。
For many years, adipose tissue was considered as an inert energy storage organ that accumulates and stores triacylglycerols during energy excess and releases fatty acids in times of systemic energy need. However, over the last two decades adipose tissue depots have been established as highly active endocrine and metabolically important organs that modulate energy expenditure and glucose homeostasis. In rodents, brown adipose tissue plays an essential role in non-shivering thermogenesis and in energy dissipation that can serve to protect against diet-induced obesity. White adipose tissue collectively referred too as either subcutaneous or visceral adipose tissue is responsible for the secretion of an array of signaling molecules, termed adipokines. These adipokines function as classic circulating hormones to communicate with other organs including brain, liver, muscle, the immune system, and adipose tissue itself. The dysregulation of adipokines has been implicated in obesity, type 2 diabetes, and cardiovascular disease. Recently, inflammatory responses in adipose tissue have been shown as a major mechanism to induce peripheral tissue insulin resistance. Although leptin and adiponectin regulate feeding behavior and energy expenditure, these adipokines are also involved in the regulation of inflammatory responses. Adipose tissue secretes various pro- and anti-inflammatory adipokines to modulate inflammation and insulin resistance. In obese humans and rodent models, the expression of pro-inflammatory adipokines is enhanced to induce insulin resistance. Collectively, these findings have suggested that obesity-induced insulin resistance may result, at least in part, from an imbalance in the expression of pro- and anti-inflammatory adipokines. Thus we will review the recent progress regarding the physiological and molecular functions of adipokines in the obesity-induced inflammation and insulin resistance with perspectives on future directions.