Chronic exposure to high fat diet triggers myelin disruption and interleukin-33 upregulation in hypothalamus

BMC Neuroscience

Sheng-Feng Tsai¹  Yu-Ming Kuo¹  Hung-Tsung Wu²  Hui-Ting Huang³  Han-Hsueh Hsieh³  Shun-Fen Tzeng³  Po-See Chen⁴  Hsin-Ying Huang⁵  Chung-Shi Yang⁵ 

[1] Department of Cell Biology and Anatomy, Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University;Department of Family Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University;Department of Life Sciences, College of Bioscience and Biotechnology, National Cheng Kung University;Department of Psychiatry, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University;Institute of Biomedical Engineering and Nanomedicine, National Health Research Institutes;

关键词: Oligodendrocytes;    Myelin;    IL-33;    Glia;    Microglia;    Obesity;   

DOI  :  10.1186/s12868-019-0516-6

来源: DOAJ

【 摘 要 】

Abstract Background Hypothalamic inflammation including astrogliosis and microglia activation occurs after intake of high fat diet (HFD) in rodent models or in obese individuals. However, the effect of chronic HFD feeding on oligodendrocytes (OLGs), a myelin-producing glial population in the central nervous system (CNS), remains unclear. In this study, we used 8-week old male C57BL/6 mice fed by HFD for 3–6 months to induce chronic obesity. Results The transmission electron microscopy imaging analysis showed that the integrity of hypothalamic myelin was disrupted after HFD feeding for 4 and 6 months. Moreover, the accumulation of Iba1+-microglia with an amoeboid hypertrophic form was continually observed in arcuate nucleus of HFD-fed mice during the entire feeding time period. Interleukin-33 (IL-33), a tissue alarmin upon injury to the CNS, was detected with an increased level in hypothalamus after HFD feeding for 3 and 4 months. Furthermore, the in vitro study indicated that exposure of mature OLGs to IL-33 impaired OLG cell structure along with a decline in the expression of myelin basic protein. Conclusions Altogether, our findings demonstrate that chronic HFD feeding triggers hypothalamic myelin disruption in accompany with IL-33 upregulation and prolonged microglial activation in hypothalamus. Given that the addition of exogenous IL-33 was harmful for the maturation of OLGs, an increase in IL-33 by chronic HFD feeding might contribute to the induction of hypothalamic myelin disruption.

【 授权许可】

Unknown