Lipodystrophy is characterized by altered partition of adipose tissue. Desp
ite heterogeneous causes, which include genetic, autoimmune and drug-induce
d forms, lipodystrophy syndromes have similar metabolic attributes, includi
ng insulin resistance, hyperlipidemia and diabetes. The mechanisms underlyi
ng the insulin resistance are unknown. One form of lipodystrophy. namely Du
nnigan-type familial partial lipodystrophy (FPLD) was shown to result from
mutations in the LMVA gene, which encodes nuclear lamins A and C. Although
the relationship between the mutations in the nuclear envelope and insulin
resistance is unclear at present these findings might eventually be shown t
o have relevance for the common insulin resistance syndrome and for drug-as
sociated lipodystrophies.