Department of Physiology, School of Medicine, Jinan University, 601 Huangpu Avenue West, Tianhe District, Guangzhou, Guangdong 510632, China.
Central Laboratory, School of Medicine, Jinan University, Guangzhou, China.
Neuropeptides. 2018 Jun;69:39-45. doi: 10.1016/j.npep.2018.04.002. Epub 2018 Apr 9.
Peroxisome proliferator-activated receptor-γ (PPARγ) regulates fatty acid storage, glucose metabolism, and food intake. Ghrelin, a gastric hormone, provides a hunger signal to the central nervous system to stimulate appetite. However, the effects of PPARγ on ghrelin production are still unclear. In the present study, the effects of PPARγ on ghrelin production were examined in lean- or high-fat diet-induced obese (DIO) C57BL/6J mice and mHypoE-42 cells, a hypothalamic cell line. 3rd intracerebroventricular injection of adenoviral-directed overexpression of PPARγ (Ad-PPARγ) reduced hypothalamic and plasma ghrelin, food intake in both lean C57BL/6J mice and diet-induced obese mice. These changes were associated with a significant increase in mechanistic target of rapamycin complex 1 (mTORC1) activity. Overexpression of PPARγ enhanced mTORC1 signaling and suppressed ghrelin production in cultured mHypoE-42 cells. Our results suggest that hypothalamic PPARγ plays a vital role in ghrelin production and food intake in mice.
过氧化物酶体增殖物激活受体-γ（PPARγ）调节脂肪酸储存、葡萄糖代谢和食物摄入。胃饥饿素是一种胃激素，向中枢神经系统发出饥饿信号，刺激食欲。然而，PPARγ 对胃饥饿素产生的影响尚不清楚。在本研究中，研究了 PPARγ 对瘦鼠或高脂肪饮食诱导肥胖（DIO）C57BL/6J 小鼠和下丘脑细胞系 mHypoE-42 中胃饥饿素产生的影响。第三次侧脑室注射腺病毒定向过表达 PPARγ（Ad-PPARγ）可减少瘦鼠和饮食诱导肥胖鼠的下丘脑和血浆胃饥饿素、食物摄入。这些变化与雷帕霉素复合物 1（mTORC1）活性的显著增加有关。过表达 PPARγ 增强了 mTORC1 信号通路，并抑制了培养的 mHypoE-42 细胞中胃饥饿素的产生。我们的结果表明，下丘脑 PPARγ 在小鼠的胃饥饿素产生和食物摄入中起着至关重要的作用。
