Source:http://linkedlifedata.com/resource/pubmed/id/10720087
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2000-3-30
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pubmed:abstractText |
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.
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pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0021-972X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
85
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1334-9
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:10720087-Adult,
pubmed-meshheading:10720087-Anthropometry,
pubmed-meshheading:10720087-Body Mass Index,
pubmed-meshheading:10720087-Fasting,
pubmed-meshheading:10720087-Fatty Acids, Nonesterified,
pubmed-meshheading:10720087-Female,
pubmed-meshheading:10720087-Genotype,
pubmed-meshheading:10720087-Heterozygote,
pubmed-meshheading:10720087-Humans,
pubmed-meshheading:10720087-Insulin Resistance,
pubmed-meshheading:10720087-Interleukin-6,
pubmed-meshheading:10720087-Lipid Metabolism, Inborn Errors,
pubmed-meshheading:10720087-Male,
pubmed-meshheading:10720087-Polymorphism, Genetic,
pubmed-meshheading:10720087-Polymorphism, Restriction Fragment Length,
pubmed-meshheading:10720087-Triglycerides
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pubmed:year |
2000
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pubmed:articleTitle |
Interleukin-6 gene polymorphism and lipid abnormalities in healthy subjects.
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pubmed:affiliation |
Unitat de Diabetologia, Endocrinologia i Nutricio, University Hospital of Girona Dr Josep Trueta, Spain. endocrino@htrueta.scs.es
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pubmed:publicationType |
Journal Article,
Clinical Trial
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