Es, insulin resistance or obesity, some studies found it to have a deleterious effect [14,42,43,44]. In Chinese population, the Ala carrier was associated with a higher fasting level of blood sugar in patients with the metabolic syndrome [35]. Similarly, the influence of the Ala carriage on metabolism in HIVinfected patients is not evident. For example, in the study by GW788388 site Saumoy et al., the Pro12Ala polymorphism had no effect on the risk of developing lipodystrophy in HIV-1-infected patients treated with HAART [45]. In the study by Nazih et al., there was no convincing association between the Pro12Ala polymorphism and individual components of the metabolic syndrome, except for the association of the Pro12Ala polymorphism with diabetes in HIV-infected patients [40]. Thus, these suggest that Pro12Ala polymorphism is unlikely to have a significant impact on the metabolic syndrome in 23727046 HIVinfected patients. Consistently, our study showed that the Ala carriers of Pro12Ala polymorphism in PPARc were not associated with serum GSK3326595 biological activity levels of cholesterol and LDL in HIV-infected patients. While the Ala carriers had higher serum cholesterol levels at several time points of the longitudinal follow-up, the borderline significance (0.04) together with insignificant power (0.54) makes the results inapplicable at a population level. We noticed relatively few Ala carriers in our study, which may be related to the insignificant impact of Ala carriage on lipid metabolism in our findings. Thus further studies with more patients are warranted to reveal the impact of Pro12Ala polymorphism on metabolism in HIV-infected patients. Because the 2803GA polymorphism is located in the enhancer region, the G.A substitution alters transcriptional efficiency and affinity of the enhancer sequence for the transcription factorHNF1a [46]. The A allele of RBP4 2803GA polymorphism was linked to an increased risk of type 2 diabetes in non HIV-infected population [21]. In HIV-infected patients receiving HAART, the serum RBP4 level has been positively correlated with obesity, insulin resistance and dyslipidemia [24]. However, the role of the A allele of RBP4 2803GA polymorphism in HIV-infected patients is still unknown. Our study revealed that the A allele of RBP4 2803GA polymorphism was associated with insulin resistance in HIV-infected patients receiving HAART. This provides us another potential surrogate marker of insulin resistance in HIVinfected patients receiving antiretroviral therapy. It has long been noted that PI treatment was associated with dyslipidemia, particularly hypertriglyceridemia [47]. The class of NNRTI, in contrast, induces dyslipidemia to a lesser degree than PI. However, NNRTI-related dyslipidemia can still be found in several studies [48,49,50]. The effect of NNRTI or PI therapy on the lipid profile of HIV-infected patients in Asia is not clear. In our study, patients with efavirenz therapy had higher serum levels of fasting glucose, LDL, and HOMA index, lower serum levels of uric acid, and more often had hypercholesterolemia and LDL.110 mg/dl, than those with lopinavir/ritonavir-based regimens. These results suggest that efavirenz may be associated with more metabolic side effects than lopinavir/ritonavir in Asian population. Thus, further randomized, double-blind trials will be required to clarify the effect of efavirenz or lopinavir/ritonavir on the metabolic profile in an Asian population. There are several limitations in our study. First, the case number is.Es, insulin resistance or obesity, some studies found it to have a deleterious effect [14,42,43,44]. In Chinese population, the Ala carrier was associated with a higher fasting level of blood sugar in patients with the metabolic syndrome [35]. Similarly, the influence of the Ala carriage on metabolism in HIVinfected patients is not evident. For example, in the study by Saumoy et al., the Pro12Ala polymorphism had no effect on the risk of developing lipodystrophy in HIV-1-infected patients treated with HAART [45]. In the study by Nazih et al., there was no convincing association between the Pro12Ala polymorphism and individual components of the metabolic syndrome, except for the association of the Pro12Ala polymorphism with diabetes in HIV-infected patients [40]. Thus, these suggest that Pro12Ala polymorphism is unlikely to have a significant impact on the metabolic syndrome in 23727046 HIVinfected patients. Consistently, our study showed that the Ala carriers of Pro12Ala polymorphism in PPARc were not associated with serum levels of cholesterol and LDL in HIV-infected patients. While the Ala carriers had higher serum cholesterol levels at several time points of the longitudinal follow-up, the borderline significance (0.04) together with insignificant power (0.54) makes the results inapplicable at a population level. We noticed relatively few Ala carriers in our study, which may be related to the insignificant impact of Ala carriage on lipid metabolism in our findings. Thus further studies with more patients are warranted to reveal the impact of Pro12Ala polymorphism on metabolism in HIV-infected patients. Because the 2803GA polymorphism is located in the enhancer region, the G.A substitution alters transcriptional efficiency and affinity of the enhancer sequence for the transcription factorHNF1a [46]. The A allele of RBP4 2803GA polymorphism was linked to an increased risk of type 2 diabetes in non HIV-infected population [21]. In HIV-infected patients receiving HAART, the serum RBP4 level has been positively correlated with obesity, insulin resistance and dyslipidemia [24]. However, the role of the A allele of RBP4 2803GA polymorphism in HIV-infected patients is still unknown. Our study revealed that the A allele of RBP4 2803GA polymorphism was associated with insulin resistance in HIV-infected patients receiving HAART. This provides us another potential surrogate marker of insulin resistance in HIVinfected patients receiving antiretroviral therapy. It has long been noted that PI treatment was associated with dyslipidemia, particularly hypertriglyceridemia [47]. The class of NNRTI, in contrast, induces dyslipidemia to a lesser degree than PI. However, NNRTI-related dyslipidemia can still be found in several studies [48,49,50]. The effect of NNRTI or PI therapy on the lipid profile of HIV-infected patients in Asia is not clear. In our study, patients with efavirenz therapy had higher serum levels of fasting glucose, LDL, and HOMA index, lower serum levels of uric acid, and more often had hypercholesterolemia and LDL.110 mg/dl, than those with lopinavir/ritonavir-based regimens. These results suggest that efavirenz may be associated with more metabolic side effects than lopinavir/ritonavir in Asian population. Thus, further randomized, double-blind trials will be required to clarify the effect of efavirenz or lopinavir/ritonavir on the metabolic profile in an Asian population. There are several limitations in our study. First, the case number is.
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