title: Interleukin-6 gene polymorphism and lipid abnormalities in healthy subjects.
abstract: Several lines of evidence indicate that interleukin-6 (IL-6) is involved not only in the hepatic acute phase response but also in adipose tissue metabolism, lipoprotein lipase activity, and hepatic triglyceride secretion. A polymorphism in the IL-6 gene, associated with differences in IL-6 transcription rate, has been recently described. We aimed to study whether this IL-6 gene polymorphism leads to differences in fasting and postglucose load plasma lipids in healthy subjects. Subjects with G at position -174 of the IL-6 gene were similar in age, sex, body mass index, and waist to hip ratio in comparison with carriers of the C allele. However, G carriers showed almost twice plasma triglycerides (1.5 +/- 0.9 vs. 0.90 +/- 0.37 mmol/L; P = 0.01), very low-density lipoprotein (VLDL)-triglycerides (0.97 +/- 0.69 vs. 0.42 +/- 0.2 mmol/L; P = 0.002), higher fasting (881 vs. 458 micromol/L; P = 0.01), and postglucose load free fatty acids (299 vs. 90.5 micromol/L; P = 0.03), slightly lower high-density lipoprotein-2 cholesterol (0.25 +/- 0.14 vs. 0.39 +/- 0.26 mmol/L; P = 0.058), and similar cholesterol and LDL-cholesterol levels than carriers of the C allele. Serum IL-6 levels correlated positively with fasting triglycerides, VLDL-triglycerides, and postload free fatty acids (r = 0.61, 0.65 and 0.60, respectively; P < 0.001) and negatively with high-density lipoprotein-cholesterol (r = -0.42, P < 0.05). A tendency toward higher serum IL-6 levels was observed among G carriers (9.9 +/- 6.9 vs. 6.85 +/- 1.7 pg/mL; P = 0.09). The -174G construct was recently reported to show higher expression of IL-6 in He La cells and was associated with higher plasma IL-6 levels than the -174C allele. Thus, the results of the present study suggest that subjects with the G allele, associated to higher IL-6 secretion, are prone to lipid abnormalities. Whether this polymorphism contributes to lipid alterations associated with other metabolic disorders awaits additional studies.
authors.affiliation: Unitat de Diabetologia, Endocrinologia i Nutricio, University Hospital of Girona Dr Josep Trueta, Spain. endocrino@htrueta.scs.es
authors.forename: J M
authors.initials: JM
authors.lastname: Fernández-Real
authors.forename: M
authors.initials: M
authors.lastname: Broch
authors.forename: J
authors.initials: J
authors.lastname: Vendrell
authors.forename: C
authors.initials: C
authors.lastname: Richart
authors.forename: W
authors.initials: W
authors.lastname: Ricart
mesh_terms: D000328:Adult; D000886:Anthropometry; D015992:Body Mass Index; D005215:Fasting / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005260:Female; D005838:Genotype; D006579:Heterozygote; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics; D015850:Interleukin-6 / Q000235:genetics*; D008052:Lipid Metabolism, Inborn Errors / Q000235:genetics*; D008297:Male; D011110:Polymorphism, Genetic / Q000235:genetics*; D012150:Polymorphism, Restriction Fragment Length; D014280:Triglycerides / Q000378:metabolism
chemical_list: D005230:Fatty Acids, Nonesterified; D015850:Interleukin-6; D014280:Triglycerides