Lipodystrophy syndromes are a group of genetic or acquired disorders in which the body is unable to produce and maintain healthy fat tissue. The medical condition is characterized by abnormal or degenerative conditions of the bodys adipose tissue. A more specific term, lipoatrophy ("lipo" is Greek for "fat", and "dystrophy" is Greek for "abnormal or degenerative condition"), is used when describing the loss of fat from one area (usually the face). This condition is also characterized by a lack of circulating leptin which may lead to osteosclerosis. The absence of fat tissue is associated with insulin resistance, hypertriglyceridemia, non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome. Types
Lipodystrophy can be divided into the following types:: 495–7 
Congenital lipodystrophy syndromes
Congenital generalized lipodystrophy (Berardinelli-Seip syndrome)
Familial partial lipodystrophy
Marfanoid–progeroid–lipodystrophy syndrome
Chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature syndrome
Acquired lipodystrophy syndromes
Acquired partial lipodystrophy (Barraquer-Simons syndrome)
Acquired generalized lipodystrophy
Centrifugal abdominal lipodystrophy (Lipodystrophia centrifugalis abdominalis infantilis)
Lipoatrophia annularis (Ferreira-Marques lipoatrophia)
Localized lipodystrophy
HIV-associated lipodystrophy

Epidemiology
Congenital lipodystrophy (due to inherited genetic defect) is estimated to be extremely rare, possibly affecting only one per million persons. Acquired lipodystrophy is much more common, especially affecting persons with HIV infection. Pathogenesis
Due to an insufficient capacity of subcutaneous adipose tissue to store fat, fat is deposited in non-adipose tissue (lipotoxicity), leading to insulin resistance. Patients display hypertriglyceridemia, severe fatty liver disease and little or no adipose tissue. Average patient lifespan is approximately 30 years before death, with liver failure being the usual cause of death.
Diagnosis
The diagnosis is a clinical diagnosis, established by an experienced endocrinologist. A genetic confirmation may be possible depending on the subtype. In up to ~40% of partial lipodystrophy patients, a causative gene has not been identified. Using a skinfold caliper to measure skinfold thickness in various parts of the body may or a total body composition scan using Dual-energy X-ray Absorptiometry may help identify the subtype. Dual-energy X-ray Absorptiometry may be useful by providing both regional %fat measurements, and direct visualization of fat distribution by means of a "fat shadow". Treatment
Leptin replacement therapy with human recombinant leptin metreleptin has been shown to be an effective therapy to alleviate the metabolic complications associated with lipodystrophy, and has been approved by the FDA for the treatment of generalized lipodystrophy syndromes. In Europe based on EMA,  metreleptin should be used in addition to diet to treat lipodystrophy, where patients have loss of fatty tissue under the skin and build-up of fat elsewhere in the body such as in the liver and muscles. The medicine is used in: adults and children above the age of two years with generalised lipodystrophy (Berardinelli-Seip syndrome and Lawrence syndrome) and in adults and children above the age of 12 years with partial lipodystrophy (including Barraquer-Simons syndrome), when standard treatments have failed.Volanesorsen is an Apo-CIII inhibitor that is currently being investigated as a potential therapeutic to reduce hypertriglycerides in Familial Partial Lipodystrophy patients in the BROADEN study.