College of Food Science and Technology, Huazhong Agricultural University, Wuhan 430070, China.
Key Laboratory of Environment Correlative Dietology, Huazhong Agricultural University, Ministry of Education, Wuhan 430070, China.
J Agric Food Chem. 2024 Nov 6;72(44):24489-24503. doi: 10.1021/acs.jafc.4c05901. Epub 2024 Oct 28.
(KGM) is used for appetite management. However, KGM's regulation of appetite through hypothalamic neurons and gut microbiota, particularly in nonobese populations, is required to be investigated. This study investigated the differential effects of KGM on appetite and energy metabolism in obese and nonobese mice. In obese mice, KGM inhibited food intake, hypothalamic inflammation, and increased energy expenditure. Conversely, in nonobese mice, KGM maintained food intake and energy expenditure but increased hypothalamic inflammation. KGM downregulated hypothalamic , , and expression and upregulated in obese mice, while it had no effect on orexigenic genes and downregulated in nonobese mice. Additionally, KGM reshaped gut microbiota and increased Short-chain fatty acids (SCFAs) formation of obese mice, where , , and , as well as SCFAs, correlated with suppressed appetite. In nonobese mice, KGM has no significant effect on SCFAs but microbes such as , , and levels were negatively correlated with hypothalamic inflammation. KGM maintains appetite and was linked to liver-derived phosphatidylcholine, countering increased hypothalamic inflammation. The differential regulation of appetite by KGM between obese and nonobese mice is associated with hypothalamic inflammatory, neuronal, and KGM-induced personalized reshaping of gut microbiota. KGM may regulate energy intake and expenditure through the microbiota-gut-brain axis.
(KGM) 用于食欲管理。然而，需要研究 KGM 通过下丘脑神经元和肠道微生物群对食欲的调节作用，特别是在非肥胖人群中。本研究调查了 KGM 对肥胖和非肥胖小鼠食欲和能量代谢的差异影响。在肥胖小鼠中，KGM 抑制了摄食、下丘脑炎症和增加了能量消耗。相反，在非肥胖小鼠中，KGM 维持了摄食和能量消耗，但增加了下丘脑炎症。KGM 在肥胖小鼠中下调了下丘脑 、 和 的表达，并上调了 ，而在非肥胖小鼠中，它对食欲刺激基因没有影响，并且下调了 。此外，KGM 重塑了肠道微生物群并增加了肥胖小鼠的短链脂肪酸 (SCFA) 形成，其中 、 、 和 ，以及 SCFA，与抑制食欲相关。在非肥胖小鼠中，KGM 对 SCFA 没有显著影响，但微生物如 、 、 和 水平与下丘脑炎症呈负相关。KGM 维持了食欲，与肝脏衍生的磷脂酰胆碱有关，可对抗增加的下丘脑炎症。KGM 在肥胖和非肥胖小鼠中对食欲的差异调节与下丘脑炎症、神经元以及 KGM 诱导的肠道微生物群个性化重塑有关。KGM 可能通过微生物群-肠道-大脑轴来调节能量摄入和消耗。
