{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["VandeKopple MJ"],"funding":["NIDDK NIH HHS","NCI NIH HHS"],"pagination":["27-38"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5567683"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["235(1)"],"pubmed_abstract":["Hypoxia-inducible lipid droplet-associated protein (HILPDA) has been shown to localize to lipid droplets in nutrient-responsive cell types such as hepatocytes and adipocytes. However, its role in the control of whole-body homeostasis is not known. We sought to measure cell-intrinsic and systemic stress responses in a mouse strain harboring whole-body Hilpda deficiency. We generated a genetically engineered mouse model of whole-body HILPDA deficiency by replacing the coding <i>Hilpda</i> exon with luciferase. We subjected the knockout animals to environmental stresses and measured whole-animal metabolic and behavioral parameters. Brown adipocyte precursors were isolated and differentiated <i>in vitro</i> to quantify the impact of HILPDA ablation in lipid storage and mobilization in these ce"],"journal":["The Journal of endocrinology"],"pubmed_title":["Stress-responsive HILPDA is necessary for thermoregulation during fasting."],"pmcid":["PMC5567683"],"funding_grant_id":["P30 CA016058","R35 CA197713","R03 CA191653","K01 DK105109","P01 CA067166"],"pubmed_authors":["Bal NC","Wu J","Maurya SK","Stanford KI","Denko NC","Periasamy M","Kalyanasundaram A","Giaccia AJ","Baer LA","Papandreou I","VandeKopple MJ"],"additional_accession":[]},"is_claimable":false,"name":"Stress-responsive HILPDA is necessary for thermoregulation during fasting.","description":"Hypoxia-inducible lipid droplet-associated protein (HILPDA) has been shown to localize to lipid droplets in nutrient-responsive cell types such as hepatocytes and adipocytes. However, its role in the control of whole-body homeostasis is not known. We sought to measure cell-intrinsic and systemic stress responses in a mouse strain harboring whole-body Hilpda deficiency. We generated a genetically engineered mouse model of whole-body HILPDA deficiency by replacing the coding <i>Hilpda</i> exon with luciferase. We subjected the knockout animals to environmental stresses and measured whole-animal metabolic and behavioral parameters. Brown adipocyte precursors were isolated and differentiated <i>in vitro</i> to quantify the impact of HILPDA ablation in lipid storage and mobilization in these ce","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Oct","modification":"2025-04-25T18:29:46.009Z","creation":"2019-06-06T17:58:53Z"},"accession":"S-EPMC5567683","cross_references":{"pubmed":["28739822"],"doi":["10.1530/joe-17-0289","10.1530/JOE-17-0289"]}}