Involvement of a battery of investigated genes in lipid droplet pathophysiology and associated comorbidities

Lipid droplets (LDs) are highly specialized energy storage organelles involved in the maintenance of lipid homoeostasis by regulating lipid flux within white adipose tissue (WAT). The physiological function of adipocytes and LDs can be compromised by mutations in several genes, leading to NEFA-induc...

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Bibliographic Details
Published in:	Adipocyte Vol. 13; no. 1; p. 2403380
Main Authors:	Al Harake, Sami N, Abedin, Yasamin, Hatoum, Fatema, Nassar, Nour Zahraa, Ali, Ali, Nassar, Aline, Kanaan, Amjad, Bazzi, Samer, Azar, Sami, Harb, Frederic, Ghadieh, Hilda E
Format:	Journal Article
Language:	English
Published:	United States Taylor & Francis 01-12-2024 Taylor & Francis Group
Subjects:	Adipocytes - metabolism adipogenesis Adipose Tissue, White - metabolism Animals Comorbidity Humans Insulin Resistance Lipid droplet formation lipid droplet hydrolysis Lipid Droplets - metabolism Lipid Metabolism - genetics lipodystrophy Lipodystrophy - genetics Lipodystrophy - metabolism Mutation Review Lipid droplet formation adipogenesis insulin resistance lipid droplet hydrolysis lipodystrophy
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Summary:	Lipid droplets (LDs) are highly specialized energy storage organelles involved in the maintenance of lipid homoeostasis by regulating lipid flux within white adipose tissue (WAT). The physiological function of adipocytes and LDs can be compromised by mutations in several genes, leading to NEFA-induced lipotoxicity, which ultimately manifests as metabolic complications, predominantly in the form of dyslipidemia, ectopic fat accumulation, and insulin resistance. In this review, we delineate the effects of mutations and deficiencies in genes - , , , , , , , , , and - involved in lipid droplet metabolism and their associated pathophysiological impairments, highlighting their roles in the development of lipodystrophies and metabolic dysfunction.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 These authors contributed equally to this work.
ISSN:	2162-3945 2162-397X 2162-397X
DOI:	10.1080/21623945.2024.2403380