Department of Nutrition Science, Purdue University, West Lafayette, Indiana;
Adipocyte Biology Lab, Pennington Biomedical Research Center, Baton Rouge, Louisiana; and Department of Biological Sciences, Louisiana State University, Baton Rouge, Louisiana
Am J Physiol Endocrinol Metab. 2015 Aug 1;309(3):E205-13. doi: 10.1152/ajpendo.00053.2015. Epub 2015 Jun 9.
Adipose tissue has the largest capacity to store energy in the body and provides energy through the release of free fatty acids during times of energy need. Different types of immune cells are recruited to adipose tissue under various physiological conditions, indicating that these cells contribute to the regulation of adipose tissue. One major pathway influenced by a number of immune cells is the release of free fatty acids through lipolysis during both physiological (e.g., cold stress) and pathophysiological processes (e.g., obesity, type 2 diabetes). Adipose tissue expansion during obesity leads to immune cell infiltration and adipose tissue remodeling, a homeostatic process that promotes inflammation in adipose tissue. The release of proinflammatory cytokines stimulates lipolysis and causes insulin resistance, leading to adipose tissue dysfunction and systemic disruptions of metabolism. This review focuses on the interactions of cytokines and other inflammatory molecules that regulate adipose tissue lipolysis during physiological and pathophysiological states.
脂肪组织具有在体内储存能量的最大能力,并在需要能量时通过释放游离脂肪酸来提供能量。在各种生理条件下,不同类型的免疫细胞被募集到脂肪组织中,这表明这些细胞有助于脂肪组织的调节。受许多免疫细胞影响的一个主要途径是在生理(例如,冷应激)和病理生理过程(例如,肥胖,2 型糖尿病)期间通过脂肪分解释放游离脂肪酸。肥胖期间脂肪组织的扩张导致免疫细胞浸润和脂肪组织重塑,这是一个促进脂肪组织炎症的平衡过程。促炎细胞因子的释放刺激脂肪分解并导致胰岛素抵抗,导致脂肪组织功能障碍和全身代谢紊乱。本综述重点介绍了细胞因子和其他炎症分子在生理和病理生理状态下调节脂肪组织脂肪分解的相互作用。