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Long‐term treatment experience in a subject with Dunnigan‐type familial partial lipodystrophy: efficacy of rosiglitazone
Author(s) -
Lüdtke A.,
Heck K.,
Genschel J.,
Mehnert H.,
Spuler S.,
Worman H. J.,
Schmidt H. H.J.
Publication year - 2005
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.2005.01757.x
Subject(s) - rosiglitazone , medicine , lmna , lipodystrophy , type 2 diabetes , endocrinology , insulin resistance , insulin , diabetes mellitus , lamin , immunology , nucleus , human immunodeficiency virus (hiv) , psychiatry , antiretroviral therapy , viral load
Dunnigan‐type familial partial lipodystrophy (FPLD) is caused by mutations in LMNA , the gene that encodes nuclear lamins A and C. FPLD is characterized by peripheral fat loss, excess central adiposity, insulin resistance, and hyperlipidaemia, which are difficult to treat. We present our 2 years’ experience of treatment with rosiglitazone in a subject with FPLD. Insulin requirement decreased significantly from 240 IU/day to 76 IU/day (range 20–240 IU/day) and serum triglyceride concentration was lowered from 13.7 ± 14.4 mmol/l to 4.5 ± 4.3 mmol/l and remained stable. Mean HbA 1c prior to rosiglitazone therapy was 9.4 ± 1.32% and decreased to 7.4 ± 0.6% during therapy with rosiglitazone. This case demonstrates the benefits of PPARγ‐agonists on glycaemic control and dyslipidaemia in a patient with FPLD. This in turn implies that PPARγ may play a pathophysiological role in FPLD.