{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Singha A"],"funding":["American Heart Association","NIA NIH HHS","National Institutes of Health","University of Texas System"],"pagination":["588447"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7538546"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11"],"pubmed_abstract":["Leptin is a potent endocrine hormone produced by adipose tissue and regulates a broad range of whole-body metabolism such as glucose and lipid metabolism, even without insulin. Central leptin signaling can lower hyperglycemia in insulin-deficient rodents via multiple mechanisms, including improvements of dyslipidemia. However, the specific neurons that regulate anti-dyslipidemia effects of leptin remain unidentified. Here we report that leptin receptors (LEPRs) in neurons expressing Cre recombinase driven by a short fragment of a promoter region of <i>Ins2</i> gene (RIP-Cre<sup>25Mgn</sup> neurons) are required for central leptin signaling to reverse dyslipidemia, thereby hyperglycemia in insulin-deficient mice. Ablation of LEPRs in RIP-Cre<sup>25Mgn</sup> neurons completely blocks glucose"],"journal":["Frontiers in endocrinology"],"pubmed_title":["Leptin Receptors in RIP-Cre<sup>25Mgn</sup> Neurons Mediate Anti-dyslipidemia Effects of Leptin in Insulin-Deficient Mice."],"pmcid":["PMC7538546"],"funding_grant_id":["RF1 AG061872"],"pubmed_authors":["Farmer S","Palavicini JP","Singha A","Han X","Fujikawa T","Sandoval D","Pan M"],"additional_accession":[]},"is_claimable":false,"name":"Leptin Receptors in RIP-Cre<sup>25Mgn</sup> Neurons Mediate Anti-dyslipidemia Effects of Leptin in Insulin-Deficient Mice.","description":"Leptin is a potent endocrine hormone produced by adipose tissue and regulates a broad range of whole-body metabolism such as glucose and lipid metabolism, even without insulin. Central leptin signaling can lower hyperglycemia in insulin-deficient rodents via multiple mechanisms, including improvements of dyslipidemia. However, the specific neurons that regulate anti-dyslipidemia effects of leptin remain unidentified. Here we report that leptin receptors (LEPRs) in neurons expressing Cre recombinase driven by a short fragment of a promoter region of <i>Ins2</i> gene (RIP-Cre<sup>25Mgn</sup> neurons) are required for central leptin signaling to reverse dyslipidemia, thereby hyperglycemia in insulin-deficient mice. Ablation of LEPRs in RIP-Cre<sup>25Mgn</sup> neurons completely blocks glucose","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020","modification":"2025-04-19T23:38:26.819Z","creation":"2025-04-19T23:38:26.819Z"},"accession":"S-EPMC7538546","cross_references":{"pubmed":["33071988"],"doi":["10.3389/fendo.2020.588447"]}}