Abstract
Background:Central obesity is a rising epidemic, and often occurs in parallel with dyslipidemia. Furthermore, enhancement of ectopic fat deposition has been observed in both human studies and animal models of altered lipidemic control. Though APOA1/C3/A4/A5 genetic polymorphisms are associated with dyslipidemia, their effect on central obesity is less known.Method:The anthropometric and metabolic parameters were taken from obese (body mass index (BMI) ⩾25 kg m−2) and non-obese healthy (BMI <25) Taiwanese patients at the initiation weight-loss intervention and 6 months later. The effects of APOA1/C3/A4/A5 genetic polymorphisms were analyzed cross-sectionally and longitudinally. Gender contributions were specifically examined.Patients:Three hundred and ninety-eight participants (obese n=262; non-obese healthy n=136) were recruited in total, and 130 obese patients underwent weight-loss treatments.Results:APOA5 rs662799 minor allele carriage was associated with unfavorable metabolic profiles in obese but not non-obese individuals at baseline. Further analysis identified gender–genotype interactions in waist-hip ratio (WHR), and that one rs662799 minor allele increased 0.032 WHR unit in obese males as analyzed by linear regression adjusted for age, BMI and plasma triglyceride (TG) (95% confidence interval (CI)=0.014–0.050, P=0.001). The rs662799-associated WHR elevation resulted in increased frequency of central obesity (WHR ⩾1.0) in rs662799 carrying obese males as analyzed by binary logistic regression adjusted for age, BMI and plasma TG (odds ratio=6.52, 95% CI=1.87–22.73, P=0.003). In contrast, APOA5 rs662799 and central obesity were no longer correlated 6 months into weight-loss treatments, owing to significant WHR reductions in male rs662799 minor allele carriers (P=0.001). Meanwhile, hypertriglyceridemia was more prevalent in both male and female obese rs662799 minor allele carriers at baseline (males, P=0.034, females, P=0.007).Conclusion:This study highlights the gender-specific and weight-sensitive effects of APOA5 rs662799 on central obesity in Taiwanese individuals, and that these effects are dyslipidemia-independent and weight-loss responsive.
Highlights
BACKGROUNDCentral obesity is a rising epidemic, and often occurs in parallel with dyslipidemia
Obesity has reached a globally epidemic level, and is forecasted to affect 800 million individuals by 2015.1,2 Prolonged obesity increases risks of developing metabolic syndrome (MetS), type 2 diabetes and cardiovascular diseases.[2]
Two hundred and sixty-two obese (BMI X25) patients and 136 non-obese (BMI o25) healthy volunteers were recruited from the Weight Management Clinic and routine health check-up in National Cheng Kung University Hospital (NCKUH) from 2007 to 2010
Summary
Central obesity is a rising epidemic, and often occurs in parallel with dyslipidemia. Though APOA1/ C3/A4/A5 genetic polymorphisms are associated with dyslipidemia, their effect on central obesity is less known. RESULTS: APOA5 rs662799 minor allele carriage was associated with unfavorable metabolic profiles in obese but not non-obese individuals at baseline. The rs662799-associated WHR elevation resulted in increased frequency of central obesity (WHR X1.0) in rs662799 carrying obese males as analyzed by binary logistic regression adjusted for age, BMI and plasma TG (odds ratio 1⁄4 6.52, 95% CI 1⁄4 1.87–22.73, P 1⁄4 0.003). APOA5 rs662799 and central obesity were no longer correlated 6 months into weight-loss treatments, owing to significant WHR reductions in male rs662799 minor allele carriers (P 1⁄4 0.001). CONCLUSION: This study highlights the gender-specific and weight-sensitive effects of APOA5 rs662799 on central obesity in Taiwanese individuals, and that these effects are dyslipidemia-independent and weight-loss responsive.
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