Single-nucleotide polymorphisms in peroxisome proliferator-activated receptor gamma and their association with plasma levels of resistin and the metabolic syndrome in a South Indian population.
Two-way ANCOVA with adjustment for age as a covariate indicated that fitness and the CC genotype of C1431T in the PPARγ2 gene interacted to produce a significant effect on MetS risk in younger men and that the risk of MetS in the CC genotype group with low cardiorespiratory fitness was significantly higher than that in the corresponding CT+TT genotypes or in the high fitness groups.
Increased expression of interleukin-1 receptor antagonist (IL-1Ra) and IL-10, a trend for higher IL-1β, and no change in peroxisome proliferator-activated receptor-γ (PPARγ) was found in EAT from MS or type 2 diabetes.Only PPARγ mRNA was reduced in SAT.
PPARγ ligands such as thiazolidinediones (TZDs) exert insulin sensitizing and anti-inflammatory effects primarily through action on adipocytes, and are thus widely used to treat metabolic syndrome, especially type II diabetes.
Peroxisome proliferator-activated receptor gamma (PPARγ) is a key regulator of adipocyte differentiation and has an important role in metabolic syndrome.
There was no convincing association between any polymorphism of PPARα and PPARγ and each individual component of the metabolic syndrome, except for the relationship of the P12A polymorphism with diabetes.
The present study suggested that the variant genotypes in PPAR-γ gene could increase the risk of MetS; however, genotypes in RXR-α gene could decrease the risk of MetS in a Chinese Han population.
The influences of PPARγ (C1431T and Pro12Ala) and RBP4 (-803GA) polymorphisms on metabolic syndrome in HIV-infected patients receiving anti-retroviral therapy were examined in this study.
In the group of participants with PPARγPro12Ala or Ala12Ala genotypes, those with the LPL Pvu (-/+) or (+/+) genotype had greater odds for MetSy (odds ratio OR=5.98; 95% confidence interval CI: 1.46-24.47, p=0.013).
We investigated the synergism between variants at the PPARγ locus (C161T and Pro12Ala polymorphisms) with insulin resistance on metabolic syndrome (MS).
The identification of fibrates and TZDs as respective ligands for PPARα and PPARγ was a groundbreaking finding that sparked notable pharmaceutical interest in PPARs as potential drug targets for treatment of the metabolic syndrome.
The aim of this study was to investigate the association of C1431T and Pro12Ala polymorphisms of PPARγ gene and their haplotypes and diplotypes with risk of metabolic syndrome (MetS) in an Iranian population.
The possible causes of metabolic syndrome by in-utero epigenetic alterations of genes involved in energy metabolism (PPARγ and PPARα), microRNAs, arginine methyltransferases, lysine demethylases, and histone deacetylaces have been elucidated.
Collectively, this study establishes a critical role of CRL4B in the regulation of PPARγ stability and insulin sensitivity and suggests that CUL4B could be a potential therapeutic target for combating obesity and metabolic syndromes.
Our data demonstrate (i) the systems-level regulatory landscape of HFD-induced metabolic syndrome involving multiple molecular parameters, including HNE, AGEs and their receptor RAGE, and (ii) attenuation of metabolic syndrome by PPARγ modulation.
Findings from the present study suggested that a sedentary lifestyle and vitamin D deficiency accelerated the occurrence of metabolic syndrome probably by decreasing the expression of nuclear receptor PPARγ.