<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Singha A</submitter><funding>American Heart Association</funding><funding>NIA NIH HHS</funding><funding>National Institutes of Health</funding><funding>University of Texas System</funding><pagination>588447</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7538546</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11</volume><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 &lt;i>Ins2&lt;/i> gene (RIP-Cre&lt;sup>25Mgn&lt;/sup> neurons) are required for central leptin signaling to reverse dyslipidemia, thereby hyperglycemia in insulin-deficient mice. Ablation of LEPRs in RIP-Cre&lt;sup>25Mgn&lt;/sup> neurons completely blocks glucose</pubmed_abstract><journal>Frontiers in endocrinology</journal><pubmed_title>Leptin Receptors in RIP-Cre&lt;sup>25Mgn&lt;/sup> Neurons Mediate Anti-dyslipidemia Effects of Leptin in Insulin-Deficient Mice.</pubmed_title><pmcid>PMC7538546</pmcid><funding_grant_id>RF1 AG061872</funding_grant_id><pubmed_authors>Farmer S</pubmed_authors><pubmed_authors>Palavicini JP</pubmed_authors><pubmed_authors>Singha A</pubmed_authors><pubmed_authors>Han X</pubmed_authors><pubmed_authors>Fujikawa T</pubmed_authors><pubmed_authors>Sandoval D</pubmed_authors><pubmed_authors>Pan M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Leptin Receptors in RIP-Cre&lt;sup>25Mgn&lt;/sup> Neurons Mediate Anti-dyslipidemia Effects of Leptin in Insulin-Deficient Mice.</name><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 &lt;i>Ins2&lt;/i> gene (RIP-Cre&lt;sup>25Mgn&lt;/sup> neurons) are required for central leptin signaling to reverse dyslipidemia, thereby hyperglycemia in insulin-deficient mice. Ablation of LEPRs in RIP-Cre&lt;sup>25Mgn&lt;/sup> neurons completely blocks glucose</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020</publication><modification>2025-04-19T23:38:26.819Z</modification><creation>2025-04-19T23:38:26.819Z</creation></dates><accession>S-EPMC7538546</accession><cross_references><pubmed>33071988</pubmed><doi>10.3389/fendo.2020.588447</doi></cross_references></HashMap>