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Epac2a-knockout mice are resistant to dexamethasone-induced skeletal muscle atrophy and short-term cold stress
Seung-Eun Song1,#, Su-Kyung Shin1,#, So-Young Park2, Il-Seon Hwang1, Seung-Soon Im1, Jae-Hoon Bae1, Myung-Sook Choi3, Dae-Kyu Song1,*
1Physiology, Keimyung University School of Medicine,
2Physiology, Yeongnam University School of Medicine,
3Department of Food Science and Nutrition, Kyungpook National University
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 sustainable 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 greater energy expenditure 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..
Abstract, Accepted Manuscript(in press) [Submitted on July 14, 2017, Accepted on November 23, 2017]
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