Epac2a-knockout mice are resistant to dexamethasone-induced skeletal muscle atrophy and short-term cold stress
| Autor: | So-Young Park, Jae-Hoon Bae, Su-Kyung Shin, Dae-Kyu Song, Ilseon Hwang, Seung-Eun Song, Myung-Sook Choi, Seung Soon Im |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
Leptin
0301 basic medicine medicine.medical_specialty Sympathetic Nervous System Hypothalamus Epac2a Skeletal muscle Adipose tissue Brown adipose tissue Biochemistry Dexamethasone Mice 03 medical and health sciences Adipose Tissue Brown Internal medicine medicine Animals Guanine Nucleotide Exchange Factors Obesity Muscle Skeletal Molecular Biology Uncoupling Protein 1 Myogenin Mice Knockout Chemistry Cold-Shock Response Sympathetic nervous activity Articles General Medicine Muscle atrophy Cold shock response 030104 developmental biology medicine.anatomical_structure Endocrinology Knockout mouse Atrophy medicine.symptom Signal Transduction |
| Zdroj: | BMB Reports |
| ISSN: | 1976-670X |
| DOI: | 10.5483/bmbrep.2018.51.1.132 |
| Popis: | 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. [BMB Reports 2018; 51(1): 39-44]. |
| Databáze: | OpenAIRE |
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