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• W2332783175 abstract "Purpose of review Adipose tissue is a key player in metabolic homeostasis through its role as an energy depot and endocrine organ. The characterization of mouse models of lipodystrophy, in which adipose tissue development and function are impaired, has shed new light on the mechanisms by which adipose tissue dysregulation may contribute to conditions such as insulin resistance, fatty liver, and β-cell toxicity. Recent findings Here we review recent findings from mouse models with genetic alterations leading to reduced adipose tissue mass. The metabolic consequences depend on the basis for the adipose tissue reduction, and we classify mouse models into three categories based on whether they confer (1) lipoatrophy accompanied by insulin resistance, (2) reduced adipose tissue storage associated with enhanced energy expenditure, or (3) both lipoatrophic and energetic effects. Summary Reductions in the capacity of adipose tissue to store triglycerides or to secrete adipokine hormones lead to altered lipid metabolism and insulin resistance. In contrast, depletion of fat stores by virtue of enhanced energy metabolism does not produce undesirable metabolic effects. However, enhanced energy metabolism cannot overcome the deleterious effects of impaired adipokine production, as revealed by studies of models with both lipoatrophic and energetic effects." @default.
• W2332783175 created "2016-06-24" @default.
• W2332783175 creator A5001478588 @default.
• W2332783175 creator A5019944871 @default.
• W2332783175 date "2006-07-01" @default.
• W2332783175 modified "2023-10-12" @default.
• W2332783175 title "Metabolic consequences of lipodystrophy in mouse models" @default.
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• W2332783175 doi "https://doi.org/10.1097/01.mco.0000232904.82038.db" @default.
• W2332783175 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16778573" @default.
• W2332783175 hasPublicationYear "2006" @default.
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