This study analyzed the mRNA expression of PPARg and nuclear factor kappa B genes in peripheral blood mononuclear cells (PBMC) from healthy control subjects and patients with the metabolic syndrome before and after a fat overload. The authors also studied the association between the Pro12 and Ala12 polymorphisms and the response of biochemical and oxidative stress parameters to a fat load. The healthy subjects showed an increased expression of PPARg after the fat overload compared to baseline level. Patients with the metabolic syndrome showed a dramatic decrease, even though the baseline expression of PPARg was lower in carriers of the Ala12 polymorphism than in carriers of the Pro12 polymorphism. Most of the indicators of oxidative stress were higher in patients with the metabolic syndrome than in healthy subjects before and after the fat overload, and significant differences in several indicators of oxidative stress between Pro12 and Ala12 carriers were found. For instance, a greater plasma carbonylated protein concentration and a lower catalase activity after the fat load in Ala12 subjects were observed. In addition, oxidative stress appeared to play a key role after the increase in circulating triglycerides, driving PPARg downregulation. The results of this study revealed that postprandial hypertriglyceridemia was associated with a fall in PPARg expression in patients with the metabolic syndrome. They also provided evidence that the Ala12 sequence variant is associated with a worse metabolic profile than Pro12.
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