Deletion of GPR30 Drives the Activation of Mitochondrial Uncoupling Respiration to Induce Adipose Thermogenesis in Female Mice

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dc.contributor.authorLuo, Jingen
dc.contributor.authorWang, Yaoen
dc.contributor.authorGilbert, Elizabeth R.en
dc.contributor.authorLiu, Dongminen
dc.date.accessioned2022-06-16T12:40:44Zen
dc.date.available2022-06-16T12:40:44Zen
dc.date.issued2022-05-03en
dc.description.abstractThermogenic adipocytes possess a promising approach to combat obesity with its capability promoting energy metabolism. We previously discovered that deletion of GPR30 (GPRKO), a presumably membrane-associated estrogen receptor, protected female mice from developing obesity, glucose intolerance, and insulin resistance when challenged with a high-fat diet (HFD). In vivo, the metabolic phenotype of wild type (WT) and GPRKO female mice were measured weekly. Acute cold tolerance test was performed. Ex vivo, mitochondrial respiration of brown adipose tissue (BAT) was analyzed from diet-induced obese female mice of both genotypes. In vitro, stromal vascular fractions (SVF) were isolated for beige adipocyte differentiation to investigate the role of GPR30 in thermogenic adipocyte. Deletion of GPR30 protects female mice from hypothermia and the mitochondria in BAT are highly energetic in GPRKO animals while the WT mitochondria remain in a relatively quiescent stage. Consistently, GPR30 deficiency enhances beige adipocyte differentiation in white adipose tissue (WAT) and activates the thermogenic browning of subcutaneous WAT due to up-regulation of UCP-1, which thereby protects female mice from HFD-induced obesity. GPR30 is a negative regulator of thermogenesis, which at least partially contributes to the reduced adiposity in the GPRKO female mice. Our findings provide insight into the mechanism by which GPR30 regulates fat metabolism and adiposity in female mice exposed to excess calories, which may be instrumental in the development of new therapeutic strategies for obesity.en
dc.description.notesThis work was partially supported by a seed grant from Virginia Tech, a grant from Diabetes Action Research and Education Foundation (USA), a grant from Virginia Tech Drug Discovery Center, and a Virginia Tech Pratt Fellowship Award.en
dc.description.sponsorshipVirginia Tech; Diabetes Action Research and Education Foundation (USA); Virginia Tech Drug Discovery Center; Virginia Tech Pratt Fellowship Awarden
dc.description.versionPublished versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.3389/fendo.2022.877152en
dc.identifier.issn1664-2392en
dc.identifier.other877152en
dc.identifier.pmid35592783en
dc.identifier.urihttp://hdl.handle.net/10919/110799en
dc.identifier.volume13en
dc.language.isoenen
dc.publisherFrontiersen
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectmitochondrial respirationen
dc.subjectthermogenesisen
dc.subjectGPR30en
dc.subjectfemale miceen
dc.subjectfatty acid oxidationen
dc.titleDeletion of GPR30 Drives the Activation of Mitochondrial Uncoupling Respiration to Induce Adipose Thermogenesis in Female Miceen
dc.title.serialFrontiers in Endocrinologyen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten

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