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

Hui Ting Huang, Sheng Feng Tsai, Hung Tsung Wu, Hsin Ying Huang, Han Hsueh Hsieh, Yu Ming Kuo, Po See Chen, Chung Shi Yang, Shun Fen Tzeng

研究成果: Article同行評審

24 引文 斯高帕斯(Scopus)


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.

期刊BMC Neuroscience
出版狀態Published - 2019 7月 10

All Science Journal Classification (ASJC) codes

  • 一般神經科學
  • 細胞與分子神經科學


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