國家衛生研究院 NHRI:Item 3990099045/10543
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    题名: High fat diet induces mitochondria stress and impairs myelin structure in rat hypothalamus
    作者: Huang, HT;Hsien, HH;Wu, HT;Tsai, SF;Huang, HY;Kuo, YM;Chen, PS;Yang, CS;Tzeng, SF
    贡献者: Institute of Biomedical Engineering and Nanomedicine
    摘要: Obesity-induced central mild inflammation and metabolic control in the hypothalamus have been well documented. Gliosis, a reactive change of astrocytes and microglia, is observed in the hypothalamus of obese rodents and humans. However, the reaction of oligodendrocytes (OLGs), a CNS myelin producing glia population, in the hypothalamus of obese individuals is poorly known. Using high-fat diet (HFD)-fed mouse model, we found that Iba1+ microglia in arcuate nucleus (ARC) and median eminence (ME) in the hypothalamus of HFD-fed mice displayed an amoeboid hypertrophic form. Interestingly, we detected an increase in the protein level of IL-27, a pleiotropic cytokine that has been recently shown to inhibit the severity of experimental autoimmune encephalomyelitis. Through comparative microRNA microarray, we observed an increase in a group of microRNAs in the hypothalamus at 3 month post HFD feeding. Among these microRNAs, we confirmed that let-7f, a regulator of brain development and glucose metabolism, was increased in the hypothalamus after HFD feeding for 4 months. Moreover, the results from transmission electron microscopy (TEM) analysis indicated that fragmented or hyperfused mitochondria was observed in the hypothalamus of HFD-fed mice. The disturbed structure of myelin in the hypothalamus of HFD-fed mice was also detected by TEM. Based on these observations, we suggest that HFD-induced mild inflammation and changes in mitochondrial functions might impair metabolism homeostasis in OLGs, and cause an injury in myelin microstructure.
    日期: 2017-06
    關聯: Glia. 2017 Jun;65(Suppl.):E207.
    Link to: http://dx.doi.org/10.1002/glia.23157
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0894-1491&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000403071700317
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