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

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Author(s)
Seung-Eun SongSu-Kyung ShinSo-Young ParkIl-Seon HwangSeung-Soon ImJae-Hoon BaeMyung-Sook ChoiDae-Kyu Song
Keimyung Author(s)
Song, Dae KyuBae, Jae HoonIm, Seung SoonHwang, 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 tissueEpac2aLeptinSkeletal muscleSympathetic 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.
Keimyung Author(s)(Kor)
송대규
배재훈
임승순
황일선
Publisher
School of Medicine (의과대학)
Citation
Seung-Eun Song et al. (2018). Epac2a knockout mice are resistant to dexamethasone-induced skeletal muscle atrophy and short-term cold stress. BMB Reports, 51(1), 39–44. doi: 10.5483/BMBRep.2018.51.1.132
Type
Article
ISSN
1976-6696
DOI
10.5483/BMBRep.2018.51.1.132
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/41237
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Pathology (병리학)
1. School of Medicine (의과대학) > Dept. of Physiology (생리학)
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