The TNF-β Gene Nco I Polymorphism Is Not Associated with Hypertriglyceridemia or Insulin Resistance in Lean and Obese Subjects

Interindividual differences in TNF-α monocyte responses can be accounted for by genetic polymorphisms at the TNF-β locus defined by theNco Irestriction enzyme. Higher triglyceride levels in non-insulin-dependent diabetic patients homozygous at the 10.5-kb fragment of the TNF-β gene have been describ...

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Published inBiochemical and biophysical research communications Vol. 236; no. 3; pp. 829 - 832
Main Authors Fernandez-Real, J.M., Gutierrez, C., Ricant, W., Casamitjana, R.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 30.07.1997
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Abstract Interindividual differences in TNF-α monocyte responses can be accounted for by genetic polymorphisms at the TNF-β locus defined by theNco Irestriction enzyme. Higher triglyceride levels in non-insulin-dependent diabetic patients homozygous at the 10.5-kb fragment of the TNF-β gene have been described. The aim of this study was to investigate whether the Ncol polymorphism of the TNF-β 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-β locus does not contribute to differences in triglyceride levels or insulin sensitivity among nondiabetic subjects.
AbstractList 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.
Interindividual differences in TNF-α monocyte responses can be accounted for by genetic polymorphisms at the TNF-β locus defined by theNco Irestriction enzyme. Higher triglyceride levels in non-insulin-dependent diabetic patients homozygous at the 10.5-kb fragment of the TNF-β gene have been described. The aim of this study was to investigate whether the Ncol polymorphism of the TNF-β 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-β locus does not contribute to differences in triglyceride levels or insulin sensitivity among nondiabetic subjects.
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.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.
Author Ricant, W.
Casamitjana, R.
Fernandez-Real, J.M.
Gutierrez, C.
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Snippet Interindividual differences in TNF-α monocyte responses can be accounted for by genetic polymorphisms at the TNF-β locus defined by theNco Irestriction enzyme....
Interindividual differences in TNF-alpha monocyte responses can be accounted for by genetic polymorphisms at the TNF-beta locus defined by the Nco I...
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StartPage 829
SubjectTerms 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
Title The TNF-β Gene Nco I Polymorphism Is Not Associated with Hypertriglyceridemia or Insulin Resistance in Lean and Obese Subjects
URI https://dx.doi.org/10.1006/bbrc.1997.7057
https://www.ncbi.nlm.nih.gov/pubmed/9245742
https://www.proquest.com/docview/79176818
Volume 236
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