Arner Peter
Department of Medicine at Karolinska Institutet, Stockholm, Sweden.
Biochimie. 2005 Jan;87(1):39-43. doi: 10.1016/j.biochi.2004.11.012.
Testosterone is a potent regulator of lipolysis by influencing catecholamine signal transduction in fat cells. Major species differences exist as regards the testosterone effect. In rodents testosterone increases beta-adrenergic receptor mediated signals to lipolysis at multiple steps in the lipolytic cascade. The sex hormone also increases alpha2-adrenoceptor antilipolytic signalling in hamster which unlike rat express this receptor in their fat cells. In humans the region of adipose tissue is critical. Visceral fat cell lipolysis is not responsive to testosterone but this sex hormone decreases catecholamine-induced lipolysis in subcutaneous fat cells due to inhibition of the expression of beta2-adrenoceptors and hormone sensitive lipase. In polycystic ovarian syndrome (PCOS), which is characterized as a hyperandrogenic state, the lipolytic effect of catecholamine is decreased in subcutaneous adipocytes due to low content of beta2-adrenoceptors and hormone sensitive lipase. It is possible that the increased testosterone levels are responsible for these abnormalities in catecholamine signal transduction in subcutaneous fat cells of PCOS women. However, in visceral fat cells of PCOS women catecholamine-induced lipolysis is enhanced which cannot be explained by testosterone.
睾酮通过影响脂肪细胞中的儿茶酚胺信号转导，成为脂肪分解的有力调节因子。关于睾酮的作用存在主要的物种差异。在啮齿动物中，睾酮在脂肪分解级联反应的多个步骤增加β-肾上腺素能受体介导的脂肪分解信号。这种性激素还增加仓鼠中α2-肾上腺素能受体的抗脂肪分解信号，与大鼠不同，仓鼠在其脂肪细胞中表达这种受体。在人类中，脂肪组织的区域至关重要。内脏脂肪细胞的脂肪分解对睾酮无反应，但这种性激素会降低皮下脂肪细胞中儿茶酚胺诱导的脂肪分解，这是由于β2-肾上腺素能受体和激素敏感性脂肪酶的表达受到抑制。在以高雄激素状态为特征的多囊卵巢综合征（PCOS）中，皮下脂肪细胞中儿茶酚胺的脂肪分解作用由于β2-肾上腺素能受体和激素敏感性脂肪酶含量低而降低。睾酮水平升高可能是PCOS女性皮下脂肪细胞中儿茶酚胺信号转导异常的原因。然而，在PCOS女性的内脏脂肪细胞中，儿茶酚胺诱导的脂肪分解增强，这无法用睾酮来解释。
