Molecular basis of partial lipodystrophy and prospects for therapy

被引:27
作者
Hegele, RA [1 ]
机构
[1] Robarts Res Inst, Blackburn Cardiovasc Genet Lab, London, ON N6A 5K8, Canada
基金
英国医学研究理事会;
关键词
D O I
10.1016/S1471-4914(01)01930-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Lipodystrophy is characterized by altered partition of adipose tissue. Despite heterogeneous causes, which include genetic, autoimmune and drug-induced forms, lipodystrophy syndromes have similar metabolic attributes, including insulin resistance, hyperlipidemia and diabetes. The mechanisms underlying the insulin resistance are unknown. One form of lipodystrophy. namely Dunnigan-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 to have relevance for the common insulin resistance syndrome and for drug-associated lipodystrophies.
引用
收藏
页码:121 / 126
页数:6
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