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论文题目: An ATF4-ATG5 signaling in hypothalamic POMC neurons regulates obesity
英文论文题目: An ATF4-ATG5 signaling in hypothalamic POMC neurons regulates obesity
第一作者: Xiao, YZ; Deng, YL; Yuan, FX; Xia, TT; Liu, H; Li, ZG; Chen, SH; Liu, ZX; Ying, H; Liu, Y; Zhai, QW; Guo, FF
英文第一作者: Xiao, YZ; Deng, YL; Yuan, FX; Xia, TT; Liu, H; Li, ZG; Chen, SH; Liu, ZX; Ying, H; Liu, Y; Zhai, QW; Guo, FF
联系作者: Guo, FF (reprint author), 320 Yueyang Rd, Shanghai 200031, Peoples R China.
英文联系作者: Guo, FF (reprint author), 320 Yueyang Rd, Shanghai 200031, Peoples R China.
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发表年度: 2017
卷: 13
期: 6
页码: 1088-1089
摘要: ATF4 (activating transcription factor 4) is an important transcription factor that has many biological functions, while its role in hypothalamic POMC (pro-opiomelanocortin-a) neurons in the regulation of energy homeostasis has not been explored. We recently discovered that mice with an Atf4 deletion specific to POMC neurons (PAKO mice) are lean and have higher energy expenditure. Furthermore, these mice are resistant to high-fat diet (HFD)-induced obesity and obesity-related metabolic disorders. Mechanistically, we found the expression of ATG5 (autophagy-related 5) is upregulated in POMC neurons of PAKO mice, and ATF4 regulates ATG5 expression by binding directly to its promoter. Mice with Atf4 and Atg5 double knockout in POMC neurons have reduced energy expenditure and gain more fat mass compared with PAKO mice under a HFD. Finally, the effect of Atf4 knockout in POMC neurons is possibly mediated by enhanced ATG5-dependent macroautophagy/autophagy and alpha-melanocyte-stimulating hormone (alpha-MSH) production in the hypothalamus. Together, this work not only identifies a beneficial role for ATF4 in hypothalamic POMC neurons in the regulation of obesity, but also provides a new potential therapeutic target for obesity and obesity-related metabolic diseases.
英文摘要: ATF4 (activating transcription factor 4) is an important transcription factor that has many biological functions, while its role in hypothalamic POMC (pro-opiomelanocortin-a) neurons in the regulation of energy homeostasis has not been explored. We recently discovered that mice with an Atf4 deletion specific to POMC neurons (PAKO mice) are lean and have higher energy expenditure. Furthermore, these mice are resistant to high-fat diet (HFD)-induced obesity and obesity-related metabolic disorders. Mechanistically, we found the expression of ATG5 (autophagy-related 5) is upregulated in POMC neurons of PAKO mice, and ATF4 regulates ATG5 expression by binding directly to its promoter. Mice with Atf4 and Atg5 double knockout in POMC neurons have reduced energy expenditure and gain more fat mass compared with PAKO mice under a HFD. Finally, the effect of Atf4 knockout in POMC neurons is possibly mediated by enhanced ATG5-dependent macroautophagy/autophagy and alpha-melanocyte-stimulating hormone (alpha-MSH) production in the hypothalamus. Together, this work not only identifies a beneficial role for ATF4 in hypothalamic POMC neurons in the regulation of obesity, but also provides a new potential therapeutic target for obesity and obesity-related metabolic diseases.
刊物名称: AUTOPHAGY
英文刊物名称: AUTOPHAGY
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学科: Cell Biology
英文学科: Cell Biology
影响因子: 8.593
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论文类别: Article
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