Epac2a knockout mice are resistant to dexamethasone-induced skeletal muscle atrophy and short-term cold stress
- Author(s)
- Seung-Eun Song; Su-Kyung Shin; So-Young Park; Il-Seon Hwang; Seung-Soon Im; Jae-Hoon Bae; Myung-Sook Choi; Dae-Kyu Song
- Keimyung Author(s)
- Song, Dae Kyu; Bae, Jae Hoon; Im, Seung Soon; Hwang, Il Seon
- Department
- Dept. of Physiology (생리학)
Dept. of Pathology (병리학)
- Journal Title
- BMB Reports
- Issued Date
- 2018
- Volume
- 51
- Issue
- 1
- Keyword
- Brown adipose tissue; Epac2a; Leptin; Skeletal muscle; Sympathetic nervous activity
- Abstract
- 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.
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