SGK1/FOXO3 Signaling in Hypothalamic POMC Neurons Mediates Glucocorticoid-Increased Adiposity
文献类型：期刊论文
| 作者 | Deng, Yalan4; Xiao, Yuzhong4; Yuan, Feixiang4; Jiang, Xiaoxue4; Deng, Jiali4; Chen, Shanghai4; Chen, Yan4; Ying, Hao4; Zhai, Qiwei4; Guo, Feifan4 |
| 刊名 | DIABETES
 |
| 出版日期 | 2018 |
| 卷号 | 67期号:4页码:569-580 |
| ISSN号 | 0012-1797 |
| 关键词 | NSCLC Cisplatin sensitivity Scribble Nox2 ROS PD-L1 |
| DOI | 10.2337/db17-1069 |
| 文献子类 | Article |
| 英文摘要 | Although the central nervous system has been implicated in glucocorticoid-induced gain of fat mass, the underlying mechanisms are poorly understood. The aim of this study was to investigate the possible involvement of hypothalamic serum- and glucocorticoid-regulated kinase 1 (SGK1) in glucocorticoid-increased adiposity. It is well known that SGK1 expression is induced by acute glucocorticoid treatment, but it is interesting that we found its expression to be decreased in the arcuate nucleus of the hypothalamus, including proopiomelanocortin (POMC) neurons, following chronic dexamethasone (Dex) treatment. To study the role of SGK1 in POMC neurons, we produced mice that developed or experienced adult-onset SGK1 deletion in POMC neurons (PSKO). As observed in Dex-treated mice, PSKO mice exhibited increased adiposity and decreased energy expenditure. Mice overexpressing constitutively active SGK1 in POMC neurons consistently had the opposite phenotype and did not experience Dex-increased adiposity. Finally, Dex decreased hypothalamic alpha-melanocyte-stimulating hormone (alpha-MSH) content and its precursor Pomc expression via SGK1/FOXO3 signaling, and intracerebroventricular injection of alpha-MSH or adenovirus-mediated FOXO3 knockdown in the arcuate nucleus largely reversed the metabolic alterations in PSKO mice. These results demonstrate that POMC SGK1/FOXO3 signaling mediates glucocorticoid-increased adiposity, providing new insights into the mechanistic link between glucocorticoids and fat accumulation and important hints for possible treatment targets for obesity. |
| 学科主题 | Endocrinology & Metabolism |
| WOS关键词 | DIET-INDUCED OBESITY ; ENERGY-EXPENDITURE ; PROOPIOMELANOCORTIN NEURONS ; LEPTIN RESISTANCE ; RAT HIPPOCAMPUS ; KINASE SGK1 ; FOOD-INTAKE ; IN-VIVO ; RECEPTOR ; MICE |
| 语种 | 英语 |
| 出版者 | AMER DIABETES ASSOC |
| WOS记录号 | WOS:000428010800006 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/556]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所 |
| 作者单位 | 1.Dartmouth Coll, Geisel Sch Med, Dept Physiol, 1 Med Ctr Dr, Lebanon, NH 03756 USA, 2.Beijing Normal Univ, Sch Brain & Cognit Sci, IDG McGovern Inst Brain Res, Beijing, Peoples R China; 3.Beijing Normal Univ, Sch Brain & Cognit Sci, State Key Lab Cognit Neurosci & Learning, Beijing, Peoples R China; 4.Univ Chinese Acad Sci, Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci,Key Lab Nutr & Metab, Shanghai, Peoples R China; |
| 推荐引用方式 GB/T 7714 | Deng, Yalan,Xiao, Yuzhong,Yuan, Feixiang,et al. SGK1/FOXO3 Signaling in Hypothalamic POMC Neurons Mediates Glucocorticoid-Increased Adiposity[J]. DIABETES,2018,67(4):569-580. |
| APA | Deng, Yalan.,Xiao, Yuzhong.,Yuan, Feixiang.,Jiang, Xiaoxue.,Deng, Jiali.,...&,.(2018).SGK1/FOXO3 Signaling in Hypothalamic POMC Neurons Mediates Glucocorticoid-Increased Adiposity.DIABETES,67(4),569-580. |
| MLA | Deng, Yalan,et al."SGK1/FOXO3 Signaling in Hypothalamic POMC Neurons Mediates Glucocorticoid-Increased Adiposity".DIABETES 67.4(2018):569-580. |
入库方式： OAI收割
来源：上海营养与健康研究所
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