TRIM67 Deficiency Exacerbates Hypothalamic Inflammation and Fat Accumulation in Obese Mice

• Published in: International journal of molecular sciences Vol. 23; no. 16; p. 9438
• Main Authors: Jia, Lanlan, Chen, Zhengli, Pan, Ting, Xia, Yu, He, Junbo, Jahangir, Asad, Wei, Xiaoli, Liu, Wentao, Shi, Riyi, Huang, Chao, Luo, Qihui
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 21.08.2022; MDPI
• Subjects: Adipose tissue; Alzheimer's disease; Apoptosis; Bioaccumulation; Body fat; Brain-derived neurotrophic factor; Cytokines; Energy; Energy balance; Energy expenditure; energy homeostasis; Food; Food intake; Genes; High fat diet; Homeostasis; Hypothalamus; Inflammation; Innervation; Lipids; Metabolic disorders; Metabolism; Nervous system; neuroinflammation; Neuropeptides; Obesity; Proteins; Rodents; Sympathetic nervous system; TRIM67
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms23169438

Obesity has achieved the appearance of a global epidemic and is a serious cause for concern. The hypothalamus, as the central regulator of energy homeostasis, plays a critical role in regulating food intake and energy expenditure. In this study, we show that TRIM67 in the hypothalamus was responsive to body-energy homeostasis whilst a deficiency of TRIM67 exacerbated metabolic disorders in high-fat-diet-induced obese mice. We found exacerbated neuroinflammation and apoptosis in the hypothalamus of obese TRIM67 KO mice. We also found reduced BDNF in the hypothalamus, which affected the fat sympathetic nervous system innervation and contributed to lipid accumulation in adipose tissue under high-fat-diet exposure. In this study, we reveal potential implications between TRIM67 and the hypothalamic function responding to energy overuptake as well as a consideration for the therapeutic diagnosis of obesity.