Relationship of abdominal adiposity and dyslipemic status in women with a common mutation in the lipoprotein lipase gene. The REGICOR investigators.
Abdominal obesity constitutes an important risk factor for cardiovascular disease. Hypertriglyceridemia and low high-density lipoprotein (HDL) cholesterol concentration constitute the major lipid alterations observed in obesity. A common variant of the lipoprotein lipase (LPL) gene, the HindIII polymorphism, has been found to be associated with changes in triglyceride and HDL-cholesterol levels. We have investigated the impact of the LPL HindIII polymorphism on the relationship between abdominal adiposity and lipoprotein concentrations in 156 randomly selected women in a cross-sectional study conducted in the province of Gerona, in the northeast of Spain. The waist-to-hip ratio was used as an estimate of regional fat distribution. Serum lipid and lipoprotein measurements as well as lipoprotein lipase-HindIII genotypes were determined. Percentile 50 of waist-to-hip ratio (WHR) (0.81) was used as a cutoff to define low or high WHR groups, which significantly differed in blood pressure and lipid trait concentrations. Serum triglyceride concentrations and mean log triglyceride-to-HDL-cholesterol ratio were significantly higher in H+ homozygous women compared with H- carriers. Whereas no statistically-significant differences were observed in HDL-cholesterol concentration and log triglyceride-to-HDL-cholesterol ratio of H- carriers between WHR groups, H+ homozygous women showed significant differences in these lipid traits. It is noteworthy that high-WHR H- carrier women showed a mean HDL-cholesterol value similar to those of both genotypes in the low WHR group. A statistically significant interaction between WHR and genotype was observed for HDL-cholesterol concentration (P=0. 027) and log triglyceride-to-HDL-cholesterol ratio (P=0.040). These results stress the compensating effects that weight loss may have on women with adverse genetic factors. From a complementary viewpoint, the presence of the H- allele seems to confer a protective lipid profile, even when an adverse anthropometric factor such as abdominal adiposity is present.
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Lipids and Cardiovascular Epidemiology Unit, Institut Municipal d'Investigació Mèdica, IMIM, Dr Aiguader 80, E-08003, Barcelona, Spain. msenti@imim.es
Bosch
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Aubó
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Elosua
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Masià
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Marrugat
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D000005:Abdomen / Q000473:pathology*; D000273:Adipose Tissue / Q000473:pathology*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001824:Body Constitution; D015992:Body Mass Index; D002318:Cardiovascular Diseases / Q000209:etiology; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D005838:Genotype; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000150:complications / Q000235:genetics*; D008071:Lipoprotein Lipase / Q000235:genetics*; D008074:Lipoproteins / Q000097:blood*; D008875:Middle Aged; D009154:Mutation; D009765:Obesity / Q000150:complications / Q000473:pathology; D011110:Polymorphism, Genetic; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
D008076:Cholesterol, HDL; D008074:Lipoproteins; D014280:Triglycerides; D002784:Cholesterol; D008071:Lipoprotein Lipase