The TNF-beta gene Nco I polymorphism is not associated with hypertriglyceridemia or insulin resistance in lean and obese subjects

Biochem Biophys Res Commun. 1997 Jul 30;236(3):829-32. doi: 10.1006/bbrc.1997.7057.

Abstract

Interindividual differences in TNF-alpha monocyte responses can be accounted for by genetic polymorphisms at the TNF-beta locus defined by the Nco I restriction enzyme. Higher triglyceride levels in non-insulin-dependent diabetic patients homozygous at the 10.5-kb fragment of the TNF-beta gene have been described. The aim of this study was to investigate whether the Ncol polymorphism of the TNF-beta gene influences the relationship between insulin resistance and triglyceride levels. Thirty-eight healthy volunteers were divided into two groups according to the absence [homozygous for class 1 allele (1/1), n=16] or presence of the class 2 allele [n=22; 19 heterozygous (1/2), and 3 homozygous (2/2)]. Both groups were comparable in sex, age, BMI, waist/hip ratio, fat mass and percentage of body fat as measured by bioelectric impedance, skinfold measurements, and blood pressure (all p>0.05). There were no differences in serum cholesterol (total, or HDL and VLDL fractions) or in total or VLDL triglycerides between the groups (all p>0.05). The insulin sensitivity index (Minimal Model method) was comparable for the two groups. In summary, the 10.5-kb homozygous genotype of the TNF-beta locus does not contribute to differences in triglyceride levels or insulin sensitivity among nondiabetic subjects.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Body Composition
  • Body Constitution
  • Body Mass Index
  • Deoxyribonucleases, Type II Site-Specific*
  • Diabetes Mellitus, Type 2 / blood
  • Diabetes Mellitus, Type 2 / genetics
  • Electric Impedance
  • Female
  • Heterozygote
  • Homozygote
  • Humans
  • Hypertriglyceridemia / genetics*
  • Insulin Resistance / genetics*
  • Lymphotoxin-alpha / genetics*
  • Male
  • Middle Aged
  • Obesity / genetics*
  • Polymorphism, Restriction Fragment Length*

Substances

  • Lymphotoxin-alpha
  • endodeoxyribonuclease NcoI
  • Deoxyribonucleases, Type II Site-Specific