School of Kinesiology and Health Science Muscle Health Research Centre, York University, Toronto, Ontario, Canada.
Metabolism. 2011 Nov;60(11):1500-10. doi: 10.1016/j.metabol.2011.06.012. Epub 2011 Aug 23.
Glucocorticoids (GCs) have long been accepted as being catabolic in nature, liberating energy substrates during times of stress to supply the increased metabolic demand of the body. The effects of GCs on adipose tissue metabolism are conflicting, however, because patients with elevated GCs present with central adiposity. We performed an extensive literature review of the effects of GCs on adipose tissue metabolism. The contradictory effects of GCs on lipid metabolism occur through a number of different mechanisms, some of which are well defined and others remain to be elucidated. Firstly, through increases in caloric and dietary fat intake, along with increased hydrolysis of circulating triglycerides (chylomicrons, very low-density lipoproteins) by lipoprotein lipase activity, GCs increase the amount of fatty acids in circulation, which are then available for ectopic fat distribution (liver, muscle, and central adipocytes). Glucocorticoids also increase de novo lipid production in hepatocytes through increased expression of fatty acid synthase. There is some controversy as to whether these same mechanisms occur in adipocytes, thereby contributing to adipose hypertrophy. Glucocorticoids promote preadipocyte conversion to mature adipocytes, causing hyperplasia of the adipose tissue. Glucocorticoids also have acute antilipolytic effect on adipocytes, whereas their genomic actions facilitate increased lipolysis after about 48 hours of exposure. The acute and long-term effects of GCs on adipose tissue lipolysis remain unclear. Although considerable evidence supports the notion that GCs increase lipolysis through glucocorticoid-induced increases of lipase expression, they clearly have antilipolytic effects within these same tissues and cell line models.
糖皮质激素（GCs）长期以来被认为具有分解代谢作用，在应激时释放能量底物，以满足身体代谢需求的增加。然而，GCs 对脂肪组织代谢的影响存在矛盾，因为升高的 GCs 水平会导致中心性肥胖。我们对 GCs 对脂肪组织代谢的影响进行了广泛的文献综述。GCs 对脂质代谢的矛盾影响是通过多种不同的机制发生的，其中一些机制已经得到很好的定义，而其他机制仍有待阐明。首先，GCs 通过增加热量和膳食脂肪的摄入，以及脂蛋白脂肪酶活性增加循环甘油三酯（乳糜微粒、极低密度脂蛋白）的水解，增加了循环中脂肪酸的量，这些脂肪酸可用于异位脂肪分布（肝脏、肌肉和中心性脂肪细胞）。GCs 还通过增加脂肪酸合酶的表达，增加肝细胞中新生脂质的产生。关于这些相同的机制是否也发生在脂肪细胞中，从而导致脂肪肥大，存在一些争议。GCs 促进前体脂肪细胞向成熟脂肪细胞的转化，导致脂肪组织增生。GCs 还对脂肪细胞具有急性抗脂解作用，而其基因组作用在暴露约 48 小时后促进脂肪分解增加。GCs 对脂肪组织脂解的急性和长期影响仍不清楚。尽管有大量证据支持 GCs 通过诱导脂肪酶表达增加来增加脂肪分解的观点，但它们在这些相同的组织和细胞系模型中显然具有抗脂解作用。
