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Sex-specific brain erythropoietin regulation of mouse metabolism and hypothalamic inflammation

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dc.contributor.author Dey, Soumyadeep
dc.contributor.author Cui, Zhenzhong
dc.contributor.author Gavrilova, Oksana
dc.contributor.author Zhang, Xiaojie
dc.contributor.author Gassmann, Max
dc.contributor.author Noguchi, Constance T.
dc.date.accessioned 2020-07-14T00:01:08Z
dc.date.available 2020-07-14T00:01:08Z
dc.date.issued 2020
dc.identifier.uri https://hdl.handle.net/20.500.12866/8278
dc.description.abstract The blood hormone erythropoietin (EPO), upon binding to its receptor (EpoR), modulates high-fat diet-induced (HFO-induced) obesity in mice, improves glucose tolerance, and prevents white adipose tissue inflammation. Transgenic mice with constitutive overexpression of human EPO solely in the brain (Tg21) were used to assess the neuroendocrine EPO effect without increasing the hematocrit. Male Tg21 mice resisted HFD-induced weight gain; showed lower serum adrenocorticotropic hormone, corticosterone, and C-reactive protein levels; and prevented myeloid cell recruitment to the hypothalamus compared with WT male mice. HFD-induced hypothalamic inflammation (HI) and microglial activation were higher in male mice, and Tg21 male mice exhibited a lower increase in HI than WT male mice. Physiological EPO function in the brain also showed sexual dimorphism in regulating HFD response. Female estrogen production blocked reduced weight gain and HI. Targeted deletion of EpoR gene expression in neuronal cells worsened HFD-induced glucose intolerance in both male and female mice but increased weight gain and HI in the hypothalamus in male mice only. Both male and female Tg21 mice kept on normal chow and HFD showed significantly improved glycemic control. Our data indicate that cerebral EPO regulates weight gain and HI in a sex-dependent response, distinct from EPO regulation of glycemic control, and independent of erythropoietic EPO response. en_US
dc.language.iso eng
dc.publisher American Society for Clinical Investigation
dc.relation.ispartof urn:issn:2379-3708
dc.rights info:eu-repo/semantics/restrictedAccess
dc.rights.uri https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
dc.subject erythropoietin en_US
dc.subject erythropoiesis en_US
dc.subject Article en_US
dc.subject controlled study en_US
dc.subject female en_US
dc.subject male en_US
dc.subject nonhuman en_US
dc.subject macrophage en_US
dc.subject animal cell en_US
dc.subject animal experiment en_US
dc.subject animal model en_US
dc.subject animal tissue en_US
dc.subject signal transduction en_US
dc.subject sex difference en_US
dc.subject encephalitis en_US
dc.subject erythropoietin receptor en_US
dc.subject protein blood level en_US
dc.subject mouse en_US
dc.subject adrenal gland en_US
dc.subject bone marrow cell en_US
dc.subject brain metabolism en_US
dc.subject brain protection en_US
dc.subject C reactive protein en_US
dc.subject cell activation en_US
dc.subject corticosterone en_US
dc.subject corticosterone blood level en_US
dc.subject corticosterone release en_US
dc.subject corticotropin en_US
dc.subject corticotropin blood level en_US
dc.subject corticotropin release en_US
dc.subject diet-induced obesity en_US
dc.subject EpoR gene en_US
dc.subject estrogen en_US
dc.subject estrogen synthesis en_US
dc.subject gene deletion en_US
dc.subject gene knockout en_US
dc.subject gene overexpression en_US
dc.subject glucose intolerance en_US
dc.subject glycemic control en_US
dc.subject hormone metabolism en_US
dc.subject hypothalamus en_US
dc.subject lipid diet en_US
dc.subject microglia en_US
dc.subject nerve cell en_US
dc.subject transgenic mouse en_US
dc.title Sex-specific brain erythropoietin regulation of mouse metabolism and hypothalamic inflammation en_US
dc.type info:eu-repo/semantics/article
dc.identifier.doi https://doi.org/10.1172/jci.insight.134061
dc.subject.ocde https://purl.org/pe-repo/ocde/ford#3.02.00 es_PE
dc.subject.ocde https://purl.org/pe-repo/ocde/ford#3.02.00

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