Peroxisome proliferator-activated receptor gamma (PPARγ) is a key regulator of adipocyte differentiation and has an important role in metabolic syndrome.
Peroxisome proliferator-activated receptor-γ (PPARγ) is a master regulator of adipogenesis, and alterations in its function are associated with various pathological processes related to metabolic syndrome.
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 genes that encode peroxisome proliferator-activated receptors (PPARs; 3 isotypes PPARalpha, PPARgamma and PPARdelta also known as PPARbeta or PPARbeta/delta), which may serve as transcriptional nodal points and therapeutic targets for metabolic syndromes, were among those affected.
The aim of this study was to evaluate the frequency of Pro12AlaPPARgamma polymorphism and its association with body mass index (BMI) and metabolic syndrome parameters in postmenopausal Polish women.
The discovery that VCE-004.8, a dual PPARγ and CB<sub>2</sub> receptor agonist, also inhibits prolyl-hydroxylases (PHDs) and activates the HIF pathway provided a rationale to investigate its effect in in vitro models of adipogenesis and in a murine model of metabolic syndrome, all processes critically regulated by these targets of VCE-004.8.
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.
We investigated the synergism between variants at the PPARγ locus (C161T and Pro12Ala polymorphisms) with insulin resistance on metabolic syndrome (MS).
The aim of this study was to determine whether MetS has an impact on the global DNA methylation pattern and the DNA methylation of several genes related to adipogenesis (PPARG, PPARA), lipid metabolism (RXRA, SREBF2, SREBF1, SCD, LPL, LXRb), and inflammation (LRP1 C3, LEP and TNF) in visceral adipose tissue.
We conclude that PPARgamma gene polymorphism may be a reliable indicator of whether exercise will have a beneficial effect as part of the treatment of insulin resistance syndrome.
Indeed, altered PPARγ transcriptional activity contributes to metabolic syndromes (obesity and hyperglycemia associated with type 2 diabetes mellitus), stroke and neurodegenerative diseases.
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.
The most prevalent human PPARgamma gene variant, Ala12, is associated with postprandial hypertriglyceridemia in patients with metabolic syndrome, although the mechanism whereby this polymorphism affects lipid homeostasis remains to be fully determined.
Angiotensin II receptor blockers with the ability to selectively modulate activity of peroxisome proliferator-activated receptor-gamma and expression of genes in these fat metabolism pathways may represent useful prototypes for a new class of transcription modulating drugs aimed at treating patients with hypertension and the metabolic syndrome.
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.