CMKLR1 deficiency attenuates androgen-inducedlipid accumulation in mice.

CMKLR1 deficiency attenuates androgen-inducedlipid accumulation in mice. Am J Physiol Endocrinol Metab. 2020 Jan 07;: Authors: Huang B, Zhao H, Huang C, Wu L, Xiang L, Wang B, Xiao T, Li M, Ren L, Niu J, Zhang J Abstract Excess androgen-induced obesity has become a public health problem, and its prevalence has increased substantially in recent years. Chemokine-like receptor 1 (CMKLR1), a receptor of Chemerin secreted by adipose tissue, is linked to adipocyte differentiation, adipose tissue development and obesity. However, the effect of CMKLR1 signaling on androgen-mediated adiposity in vivo remains unclear. Here, using pharmacological method, orchidectomized model and CMKLR1 knockout mice, we demonstrated that androgen excess in female mice resulted in a larger cell size in white adipose tissue (WAT) and brown adipose tissue (BAT), whereas androgen deprivation of male mice induced a smaller cell size. Both effects relating to the adipocytes size were both attenuated in CMKLR1 knockout mice. CMKLR1 deficiency influenced the effect of androgen on adipose tissue by regulating the mRNA expression of androgen receptor (AR) and adipocyte markers (such as Fabp4 and Cidea). Moreover, in vivo suppression of CMKLR1 by its antagonist α-NETA can also weaken the enlargement of the adipocyte cell size caused by 5α-dihydrotestosterone (DHT). Furthermore, using in vitro BAT explants culture and PI3K signaling antagonist wortmannin, we found DHT c...
Source: Am J Physiol Endocri... - Category: Endocrinology Authors: Tags: Am J Physiol Endocrinol Metab Source Type: research