Metabolic consequences of lipodystrophy in mouse modelsReue, Karena,b,c; Phan, JackaCurrent Opinion in Clinical Nutrition & Metabolic Care: July 2006 - Volume 9 - Issue 4 - p 436–441 doi: 10.1097/01.mco.0000232904.82038.db Nutrition in wasting disease Abstract Author Information 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. Author Information aDepartments of Human Genetics, USA bMedicine, David Geffen School of Medicine at UCLA, USA cVeterans Administration Greater Los Angeles Healthcare System, Los Angeles, California, USA Correspondence to Karen Reue, Department of Human Genetics, Gonda Center 6506A, Charles E. Young Drive, University of California, Los Angeles, CA 90095, USA Tel: +1 310 268 4649; fax: +1 310 268 4981; e-mail: firstname.lastname@example.org © 2006 Lippincott Williams & Wilkins, Inc.