Her regions of the gene that regulate the activity of PPARc

Her regions of the gene that regulate the activity of PPARc [16]. The estimated frequencies of PPARc Pro12Ala and C1431T polymorphisms in Chinese are about 7.2 and 44.3 [17]. Retinol-binding protein 4 (RBP4) is an adipocytokine, secreted from adipocytes and released into circulation [18]. Serum RBP4 levels are elevated in insulin-resistant mice and humans with obesity and type 2 diabetes, and are normalized by rosiglitazone, a PPARc agonist [19]. Experiments in mice indicated that elevated RBP4 levels cause insulin resistance, suggesting that the improvement of glucose metabolism by PPARc activation may be through the reduction of circulating RBP4 levels [20]. Furthermore, RBP4 2803GA polymorphism (rs3758539), located at 59 upstream of the translational start site within a putative enhancer region, is associated with an increased risk of type 2 diabetes in non HIVinfected patients [21]. In vitro studies showed that 2803 A allele PHCCC induces greater transcriptional activity and higher binding affinity with the transcription factor hepatocyte nuclear factor 1 alpha (HNF1a) than the G allele, which may cause increased serum RBP4 levels in diabetic patients [22,23]. Antiretroviral therapy in HIV-infected patients has been reported to induce a pronounced Dimethylenastron increase of plasma RBP4 [18], which is associated with obesity, insulin resistance and dyslipidemia [24]. However, the relationship between PPARc or RBP4 polymorphism and insulin resistance or dyslipidemia in HIV-infected patients receiving HAART remains unclear. The objective of the present study is to investigate the effect of PPARc and RBP4 polymorphisms on body mass, insulin resistance and dyslipidemia among HIV-infected patients with anti-retroviral therapy after adjusting other risk factors, including influence of anti-retroviral regimen, diet and drinking.Materials and MethodsA cross-sectional study of HIV-1 infected patients in the National Cheng Kong University Hospital was conducted. HIVinfected patients aged 18 years or older with regular outpatient follow-ups and antiretroviral therapy (efavirenz or lopinavir/ ritonavir plus two nucleoside reverse transcriptase inhibitors [NRTIs]) for at least one year were included. Patients, who had diabetes mellitus (DM), dyslipidemia or lipodystrophy before the clinical diagnosis of HIV infection, or had active opportunistic infections, were excluded. Demographic data, duration of HIV disease, regimen and 18325633 duration of HAART were collected. Body height, body weight, waist and hip circumference, and blood pressure were measured at outpatient visits. The waist circumference was measured at the midpoint of the rib margin and the iliac crest at the end of expiration, and the hip circumference was measured at the greatest protuberance of the buttocks [25]. Central obesity was defined as waist .90 cm for men and .80 cm for women according to the Bureau of Health Promotion, Department of Health, Taiwan. The diet condition and habitual of the patients were assessed by a modified questionnaire [26,27]. The nutrition content of the diet was analyzed. Daily metabolic rate and total energy consumption in calories (including resting energy expenditure and total energy expenditure [TEE]) were calculated from age, gender, weight and height of the patients [26]. Patients who ate more than TEE were regarded as intake over-TEE, otherwise under-TEE. Overnight fasting blood samples were taken for the measurement of serum concentrations of glucose, insulin, triglycer.Her regions of the gene that regulate the activity of PPARc [16]. The estimated frequencies of PPARc Pro12Ala and C1431T polymorphisms in Chinese are about 7.2 and 44.3 [17]. Retinol-binding protein 4 (RBP4) is an adipocytokine, secreted from adipocytes and released into circulation [18]. Serum RBP4 levels are elevated in insulin-resistant mice and humans with obesity and type 2 diabetes, and are normalized by rosiglitazone, a PPARc agonist [19]. Experiments in mice indicated that elevated RBP4 levels cause insulin resistance, suggesting that the improvement of glucose metabolism by PPARc activation may be through the reduction of circulating RBP4 levels [20]. Furthermore, RBP4 2803GA polymorphism (rs3758539), located at 59 upstream of the translational start site within a putative enhancer region, is associated with an increased risk of type 2 diabetes in non HIVinfected patients [21]. In vitro studies showed that 2803 A allele induces greater transcriptional activity and higher binding affinity with the transcription factor hepatocyte nuclear factor 1 alpha (HNF1a) than the G allele, which may cause increased serum RBP4 levels in diabetic patients [22,23]. Antiretroviral therapy in HIV-infected patients has been reported to induce a pronounced increase of plasma RBP4 [18], which is associated with obesity, insulin resistance and dyslipidemia [24]. However, the relationship between PPARc or RBP4 polymorphism and insulin resistance or dyslipidemia in HIV-infected patients receiving HAART remains unclear. The objective of the present study is to investigate the effect of PPARc and RBP4 polymorphisms on body mass, insulin resistance and dyslipidemia among HIV-infected patients with anti-retroviral therapy after adjusting other risk factors, including influence of anti-retroviral regimen, diet and drinking.Materials and MethodsA cross-sectional study of HIV-1 infected patients in the National Cheng Kong University Hospital was conducted. HIVinfected patients aged 18 years or older with regular outpatient follow-ups and antiretroviral therapy (efavirenz or lopinavir/ ritonavir plus two nucleoside reverse transcriptase inhibitors [NRTIs]) for at least one year were included. Patients, who had diabetes mellitus (DM), dyslipidemia or lipodystrophy before the clinical diagnosis of HIV infection, or had active opportunistic infections, were excluded. Demographic data, duration of HIV disease, regimen and 18325633 duration of HAART were collected. Body height, body weight, waist and hip circumference, and blood pressure were measured at outpatient visits. The waist circumference was measured at the midpoint of the rib margin and the iliac crest at the end of expiration, and the hip circumference was measured at the greatest protuberance of the buttocks [25]. Central obesity was defined as waist .90 cm for men and .80 cm for women according to the Bureau of Health Promotion, Department of Health, Taiwan. The diet condition and habitual of the patients were assessed by a modified questionnaire [26,27]. The nutrition content of the diet was analyzed. Daily metabolic rate and total energy consumption in calories (including resting energy expenditure and total energy expenditure [TEE]) were calculated from age, gender, weight and height of the patients [26]. Patients who ate more than TEE were regarded as intake over-TEE, otherwise under-TEE. Overnight fasting blood samples were taken for the measurement of serum concentrations of glucose, insulin, triglycer.