Lipodystrophic Syndrome

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Diabetes with lipodystrophy comprises a heterogeneous group of rare syndromes characterised by insulin-resistant diabetes mellitus associated with an absence of subcutaneous adipose tissue.

Several types of lipodystrophy have been reported and are distinguished according to mode of inheritance, and extent and regional distribution of fat loss. Patients with congenital lipoat-rophic diabetes demonstrate insulin resistance, elevated BMR, and hepatomegaly. The absence of subcutaneous fat is noted in early infancy, although the diabetes typically appears later, with a mean onset at 12 years. In acquired generalised lipodystrophy, clinical diabetes typically follows the onset of lipoatrophy by an average of 4 years. Although acquired lipodystrophy in human immunodeficiency virus (HlV)-infected patients is the most prevalent type of lipodystrophy, the development of hyperglycaemia appears to be uncommon [34].

The mechanisms of insulin resistance and metabolic complications in patients with lipodys-trophies are unclear. These features are observed in patients with various types of lipodystrophy and in several animal models. Since the extent of fat loss determines the severity of the complications, a common mechanism seems likely. Only limited quantities of triglycerides can be stored in unaffected fat depots in patients with marked fat loss. Excess triglycerides may then accumulate in the liver and skeletal muscles, contributing to insulin resistance. Although hyperinsulinaemia may initially compensate for insulin resistance and maintain euglycaemia, gradual progression of beta-cell dysfunction can lead to overt hypergly-caemia [35].

Recently, Oral et al. [36] reported that treatment with recombinant leptin was safe and effective in the treatment of lipodystrophy. Fasting blood glucose and glycosylated haemoglobin values decreased markedly after 4 months of therapy in the eight patients with diabetes, and serum triglyceride levels declined in all nine with lipodystrophies. Leptin therapy appeared to reduce hepatic steatosis, decrease intramyocellular lipid contents, and improve insulin sensitivity [37,38].

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