Publication details

Polymorphism NcoI in tumor necrosis factor b is associated with fasting glycemia and lipid parameters in healthy non-obese Caucasian subjects: Preliminary report

Authors

KAŇKOVÁ Kateřina MÁROVÁ Ivana JANSEN Eugene HJM VAŠKŮ Anna JURAJDA Michal VÁCHA Jiří

Year of publication 2002
Type Article in Periodical
Magazine / Source Diabetes & Metabolism
MU Faculty or unit

Faculty of Medicine

Citation
Field Endocrinology, diabetology, metabolism, nutrition
Keywords Type 2 diabetes mellitus; TNF-b polymorphism; insulin resistance; glycemia; glucose intolerance
Description Background: The study was designed to investigate the associations among polymorphisms TNF-b NcoI and TNF-a -308G/A, plasma TNF-a levels and metabolic and anthropometric parameters related to insulin sensitivity in a set of 113 Caucasian subjects undergoing oral glucose tolerance test (oGTT). Methods: Genotypes were detected by PCR; BMI, WHR, glycemia during oGTT, fasting immunoreactive insulin, fasting C-peptide, HbA1c, total cholesterol, triglycerides, HDL, LDL and plasma TNF-a levels were measured in each subject. Results: Type 2 diabetes was diagnosed in 10 subjects, impaired glucose tolerance (IGT) in 41, normal glucose tolerance (NGT) in 62. Significant differences among genotypes of the TNF-b NcoI were observed for FPG (P=0.0063), LDL (P=0.0179) and marginally for total cholesterol (P=0.0763) in NGT group. After the classification of NGT subjects into obese and non-obese according to BMI, associations of TNF-b NcoI with FPG, LDL and cholesterol were proved in non-obese subgroup only. TNF-a -308G/A polymorphism was not associated with any of the parameters studied. TNF-a levels did not revealed difference among NGT, IGT and DM groups or genotype-dependent differences. Conclusions: Our results indicate significant association of the TNF-b NcoI polymorphism with FPG, LDL and total cholesterol in normoglycemic non-obese Caucasian subjects. This polymorphism could be involved in genetic modulation of glucose and lipid homeostasis and regulation of insulin sensitivity already in healthy state. Disturbances of this regulation could be component of pathogenesis of type 2 diabetes mellitus.
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