Epac2a-knockout mice are resistant to dexamethasone-induced skeletal muscle atrophy and short-term cold stress

BMB Reports

Il-Seon Hwang^1¹  Seung-Eun Song^1²  So-Young Park^2³  Su-Kyung Shin^1⁴ 

[1]Department of Food Science and Nutrition, Kyungpook National University, Daegu 41566, Korea^4

[2]Department of Physiology &^1

[3]Department of Physiology, Yeungnam University School of Medicine, Daegu 42415, Korea^3

[4]Obesity-mediated Disease Research Center, Keimyung University School of Medicine, Daegu 82601, Korea^2

关键词: Brown adipose tissue;   

DOI  :  10.5483/BMBRep.2018.51.1.132

学科分类：生物化学/生物物理

来源: Korean Society for Biochemistry and Molecular Biology

【 摘 要 】

Exchange protein directly activated by cAMP (Epac) 2a-knockout (KO) mice exhibit accelerated diet-induced obesity and are resistant to leptin-mediated adipostatic signaling from the hypothalamus to adipose tissue, with sustained food intake. However, the impact of Epac2a deficiency on hypothalamic regulation of sympathetic nervous activity (SNA) has not been elucidated. This study was performed to elucidate the response of Epac2a-KO mice to dexamethasone-induced muscle atrophy and acute cold stress. Compared to age-matched wild-type mice, Epac2a-KO mice showed higher energy expenditures and expression of myogenin and uncoupling protein-1 in skeletal muscle (SM) and brown adipose tissue (BAT), respectively. Epac2a-KO mice exhibited greater endurance to dexamethasone and cold stress. In wild-type mice, exogenous leptin mimicked the responses observed in Epac2a-KO mice. This suggests that leptin-mediated hypothalamic signaling toward SNA appears to be intact in these mice. Hence, the potentiated responses of SM and BAT may be due to their high plasma leptin levels.

【 授权许可】

Unknown