The exact pathophysiologic mechanism is mostly unknown; however, each of three main origins, autoimmune, panniculitis, or idiopathic, may have different mechanisms of pathogenesis. Normally, adipose tissues contain adipocytes to store fat for energy during fasting period and release leptin to regulate homeostasis of energy and sensitize insulin. In AGL patients, adipose tissues are insufficient and leads to fat deposition in non-adipose tissues, such as muscle or liver, resulting in hypertriglyceridemia. Continuous elevation in triglyceride levels further contributes to metabolic problems including insulin resistance. As the level of leptin in the body is proportional to the amount of adipose tissue present, AGL patients also have a deficiency of leptin which contributes to excessive eating and worsens the metabolic syndrome. In a few patients with AGL, the presence of antibodies against adipocyte has been identified.
Acquired generalized lipodystrophy
Drug-induced lipodystrophy
Involutional lipoatrophy
Congenital generalized lipodystrophy
Familial partial lipodystrophy
Lipoatrophic diabetes
Oral galvanism
HIV-associated lipodystrophy