<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Grover A</submitter><funding>Intramural NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>National Institute of Diabetes and Digestive and Kidney Diseases</funding><pagination>e4163-e4178</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8475236</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>106(10)</volume><pubmed_abstract>&lt;h4>Context&lt;/h4>Leptin is an adipokine that signals energy sufficiency. In rodents, leptin deficiency decreases energy expenditure (EE), which is corrected following leptin replacement. In humans, data are mixed regarding leptin-mediated effects on EE.&lt;h4>Objective&lt;/h4>To determine the effects of metreleptin on EE in patients with lipodystrophy.&lt;h4>Design, setting, and patients&lt;/h4>Nonrandomized crossover study of 25 patients with lipodystrophy (National Institutes of Health, 2013-2018).&lt;h4>Intervention&lt;/h4&gt;The initiation cohort consisted of 17 patients without prior exposure to metreleptin, studied before and after 14 days of metreleptin. The withdrawal cohort consisted of 8 previously metreleptin-treated patients, studied before and after 14 days of metreleptin withdrawal.&lt;h4>Main outcom</pubmed_abstract><journal>The Journal of clinical endocrinology and metabolism</journal><pubmed_title>Leptin Decreases Energy Expenditure Despite Increased Thyroid Hormone in Patients With Lipodystrophy.</pubmed_title><pmcid>PMC8475236</pmcid><funding_grant_id>R01 DK071013</funding_grant_id><funding_grant_id>ZIA DK071013</funding_grant_id><funding_grant_id>DK075084-08</funding_grant_id><funding_grant_id>ZIA DK075084</funding_grant_id><pubmed_authors>Quaye E</pubmed_authors><pubmed_authors>Christensen J</pubmed_authors><pubmed_authors>Grover A</pubmed_authors><pubmed_authors>Meehan CA</pubmed_authors><pubmed_authors>Valencia A</pubmed_authors><pubmed_authors>Marshall B</pubmed_authors><pubmed_authors>Brychta RJ</pubmed_authors><pubmed_authors>Chen KY</pubmed_authors><pubmed_authors>Startzell MS</pubmed_authors><pubmed_authors>Brown RJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Leptin Decreases Energy Expenditure Despite Increased Thyroid Hormone in Patients With Lipodystrophy.</name><description>&lt;h4>Context&lt;/h4>Leptin is an adipokine that signals energy sufficiency. In rodents, leptin deficiency decreases energy expenditure (EE), which is corrected following leptin replacement. In humans, data are mixed regarding leptin-mediated effects on EE.&lt;h4>Objective&lt;/h4>To determine the effects of metreleptin on EE in patients with lipodystrophy.&lt;h4>Design, setting, and patients&lt;/h4>Nonrandomized crossover study of 25 patients with lipodystrophy (National Institutes of Health, 2013-2018).&lt;h4>Intervention&lt;/h4&gt;The initiation cohort consisted of 17 patients without prior exposure to metreleptin, studied before and after 14 days of metreleptin. The withdrawal cohort consisted of 8 previously metreleptin-treated patients, studied before and after 14 days of metreleptin withdrawal.&lt;h4>Main outcom</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Sep</publication><modification>2025-04-04T22:33:44.903Z</modification><creation>2025-02-19T03:24:12.978Z</creation></dates><accession>S-EPMC8475236</accession><cross_references><pubmed>33890058</pubmed><doi>10.1210/clinem/dgab269</doi></cross_references></HashMap>