The human peroxisome proliferator-activated receptor gamma2 (PPARgamma2) Pro12Ala polymorphism is associated with decreased risk of diabetic nephropathy in patients with type 2 diabetes.
The genetic influence of PPARGP12A genotype is modest and is overshadowed by duration of diabetes and systolic blood pressure as the major risk factors for diabetic nephropathy in the Oji-Cree population.
The genetic influence of PPARG P12A genotype is modest and is overshadowed by duration of diabetes and systolic blood pressure as the major risk factors for diabetic nephropathy in the Oji-Cree population.
We aim to investigate Turkish type 2 diabetic patients with/without diabetic nephropathy and healthy group and examined the contribution of the G/C exon 2 and T/C exon 6 of the PPAR gamma gene polymorphism to the development of diabetic nephropathy.
In the present study, we investigated the effect and molecular mechanism of the PPARgamma agonist, pioglitazone, on the progression of diabetic nephropathy in type 2 diabetic rats.
We examined the relationship between two PPAR-gamma gene polymorphisms, namely the P12A and C161T, and cardiovascular disease in patients with diabetic nephropathy.
We conclude that P12A and C161T polymorphisms of the PPAR-gamma gene are important predictors of cardiovascular event in patients with diabetic nephropathy.
The Pro12Ala polymorphism in the peroxisome proliferator-activated receptor-gamma 2 gene is suggested to associate with diabetic nephropathy and cardiovascular disease in type 2 diabetes.
Association and interaction analyses of genetic variants in ADIPOQ, ENPP1, GHSR, PPARgamma and TCF7L2 genes for diabetic nephropathy in a Taiwanese population with type 2 diabetes.
EGFR inhibition may be a therapeutic strategy in the treatment of diabetic nephropathy and in limiting salt and water retention, which currently restricts the use of PPARγ agonists.
The aim of the present study is to identify the regulation of lncRNA TUG1 on extracellular matrix accumulation via mediating microRNA-377 targeting of PPARγ, and investigate the underlying mechanisms in progression of DN.
Thus, in line with the role of PPARγ in metabolic homeostasis, Pparg null-mice first represent a potent model for studying the initiation and the development of diabetic nephropathy.
Peroxisome proliferator activated receptor-gamma (PPAR-γ) is implicated in several metabolic syndromes including Diabetic Nephropathy, besides obesity, insulin insensitivity, dislipidemia, inflammation, and hypertension.
To investigate this hypothesis, db/db diabetic mice were used to establish a DKD model and the PPARγ agonist rosiglitazone was employed to induce PGC‑1α expression in vivo.