RA Hegele, H Cao, C Frankowski, ST Mathews, T Leff - Diabetes, 2002 - Am Diabetes Assoc Autosomal dominant familial partial lipodystrophy (FPLD) due to mutant LMNA encoding nuclear
lamin A/C is characterized by adipose tissue repartitioning together with multiple metabolic
disturbances, including insulin resistance and dyslipidemia. There is emerging evidence ... Cited by 158 - Related articles - BL Direct - All 6 versions
AK Agarwal, A Garg - Journal of Clinical Endocrinology & Metabolism, 2002 - Endocrine Soc Familial partial lipodystrophies (FPL) are a heterogeneous group of genetic disorders characterized
by marked loss of subcutaneous (sc) fat from the extremities. Affected individuals show an increased
preponderance of insulin resistance, diabetes mellitus and dyslipidemia. Recently, lamin ... Cited by 167 - Related articles - All 4 versions
- ►diabetesjournals.org DB Savage, GD Tan, CL Acerini, SA Jebb, M Agostini, … - Diabetes, 2003 - Am Diabetes Assoc We previously reported a syndrome of severe hyperinsulinemia and early-onset hypertension
in three patients with dominant-negative mutations in the nuclear hormone receptor peroxisome
proliferator-activated receptor (PPAR)-γ. We now report the results of further detailed ... Cited by 212 - Related articles - BL Direct - All 6 versions
- ►endojournals.org M Agostini, M Gurnell, DB Savage, EM Wood, AG Smith … - Endocrinology, 2004 - Endocrine Soc Loss-of-function mutations in the ligand-binding domain of human peroxisome proliferator-activated
receptor (PPAR ) are associated with a novel syndrome characterized by partial lipodystrophy
and severe insulin resistance. Here we have further characterized the properties of ... Cited by 54 - Related articles - BL Direct - All 4 versions
- ►endojournals.org K Al-Shali, H Cao, N Knoers, AR Hermus, CJ … - Journal of Clinical …, 2004 - Endocrine Soc Familial partial lipodystrophy (FPLD) results from coding sequence mutations either in
LMNA, encoding nuclear lamin A/C, or in PPARG, encoding peroxisome proliferator-activated
receptor (PPAR ). The LMNA form is called FPLD2 (MIM 151660), and the PPARG form is ... Cited by 34 - Related articles - BL Direct - All 6 versions
- ►nih.gov YS Tsai, HJ Kim, N Takahashi, HS Kim, JR … - Journal of Clinical …, 2004 - Am Soc Clin Investig Peroxisome proliferator–activated receptor γ (PPARγ), the molecular target of a class of insulin
sensitizers, regulates adipocyte differentiation and lipid metabolism. A dominant negative P467L
mutation in the ligand-binding domain of PPARγ in humans is associated with severe ... Cited by 81 - Related articles - BL Direct - All 10 versions
- ►nih.gov M Agostini, E Schoenmakers, C Mitchell, I Szatmari, D … - Cell Metabolism, 2006 - Elsevier PPARγ is essential for adipogenesis and metabolic homeostasis. We describe mutations in the
DNA and ligand binding domains of human PPARγ in lipodystrophic, severe insulin
resistance. These receptor mutants lack DNA binding and transcriptional activity but can ... Cited by 42 - Related articles - All 11 versions
I Barroso, M Gurnell, VEF Crowley, M Agostini, JW … - Nature, 1999 - nature.com Thiazolidinediones are a new class of antidiabetic agent that improve insulin sensitivity and reduce
plasma glucose and blood pressure in subjects with type 2 diabetes 1 . Although these agents
can bind and activate an orphan nuclear receptor, peroxisome proliferator-activated ... Cited by 750 - Related articles - BL Direct - All 7 versions
- ►nih.gov AW Norris, L Chen, SJ Fisher, I Szanto, M … - Journal of Clinical …, 2003 - Am Soc Clin Investig Activation of peroxisome proliferator-activated receptor γ (PPARγ) by thiazolidinediones
(TZDs) improves insulin resistance by increasing insulin-stimulated glucose disposal in skeletal
muscle. It remains debatable whether the effect of TZDs on muscle is direct or indirect via ... Cited by 209 - Related articles - BL Direct - All 6 versions
