{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ji L"],"funding":["National Natural Science Foundation of China"],"pagination":["2002794"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7967052"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(6)"],"pubmed_abstract":["Altering the balance between energy intake and expenditure is a major strategy for treating obesity. Nonetheless, despite the progression in antiobesity drugs on appetite suppression, therapies aimed at increasing energy expenditure are limited. Here, knockout of<i>AKAP1</i>, a signaling hub on outer mitochondrial membrane, renders mice resistant to diet-induced obesity.<i>AKAP1</i> knockout significantly enhances energy expenditure and thermogenesis in brown adipose tissues (BATs) of obese mice. Restoring AKAP1 expression in BAT clearly reverses the beneficial antiobesity effect in <i>AKAP1<sup>-/-</sup></i> mice. Mechanistically, AKAP1 remarkably decreases fatty acid β-oxidation (FAO) by phosphorylating ACSL1 to inhibit its activity in a protein-kinase-A-dependent manner and thus inhibit"],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["<i>AKAP1</i> Deficiency Attenuates Diet-Induced Obesity and Insulin Resistance by Promoting Fatty Acid Oxidation and Thermogenesis in Brown Adipocytes."],"pmcid":["PMC7967052"],"funding_grant_id":["81870284","81830070","81772935"],"pubmed_authors":["Li F","Ji L","Wang G","He L","Huang Q","Zhao Y","Kang F","Xing J","He Y","Guo H","Qi B","Zhao J","Liu F","Gao T"],"additional_accession":[]},"is_claimable":false,"name":"<i>AKAP1</i> Deficiency Attenuates Diet-Induced Obesity and Insulin Resistance by Promoting Fatty Acid Oxidation and Thermogenesis in Brown Adipocytes.","description":"Altering the balance between energy intake and expenditure is a major strategy for treating obesity. Nonetheless, despite the progression in antiobesity drugs on appetite suppression, therapies aimed at increasing energy expenditure are limited. Here, knockout of<i>AKAP1</i>, a signaling hub on outer mitochondrial membrane, renders mice resistant to diet-induced obesity.<i>AKAP1</i> knockout significantly enhances energy expenditure and thermogenesis in brown adipose tissues (BATs) of obese mice. Restoring AKAP1 expression in BAT clearly reverses the beneficial antiobesity effect in <i>AKAP1<sup>-/-</sup></i> mice. Mechanistically, AKAP1 remarkably decreases fatty acid β-oxidation (FAO) by phosphorylating ACSL1 to inhibit its activity in a protein-kinase-A-dependent manner and thus inhibit","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Mar","modification":"2025-04-18T13:27:28.364Z","creation":"2025-04-06T23:13:11.65Z"},"accession":"S-EPMC7967052","cross_references":{"pubmed":["33747723"],"doi":["10.1002/advs.202002794"]}}