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Tumour necrosis factor β alleles and hyperinsulinaemia in coronary artery disease
Author(s) -
; Braun,
März,
Winkelmann,
Donner,
Henning Usadel,
Badenhoop
Publication year - 1998
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.1998.00334.x
Subject(s) - medicine , coronary artery disease , endocrinology , diabetes mellitus , loss of heterozygosity , allele , insulin , tumor necrosis factor alpha , risk factor , metabolic syndrome , biology , gene , genetics
Background Hyperinsulinaemia and dyslipoproteinaemia are markers and risk factors for coronary artery disease (CAD) and non‐insulin‐dependent diabetes mellitus (NIDDM). We investigated the influence of a tumour necrosis factor β (TNF‐β) gene polymorphism on serum parameters related to these metabolic disorders in patients with CAD. Methods A total of 199 patients with CAD and 81 control subjects with angiographically normal coronary arteries were studied. A digestion of amplified DNA with Nco I revealed three fragment patterns: homozygosity for TNF‐β*1 or TNF‐β*2 and heterozygosity (TNF‐β*1/*2). Results Patients with CAD who had increased serum insulin or C‐peptide (fasting and after glucose load) were predominantly heterozygous for TNF‐β (72% vs. 47%) and less frequently homozygous for TNF‐β*2 (22% vs. 43%, P = 0.03). Conclusion This study demonstrates an association of TNF‐β alleles with the risk factor hyperinsulinaemia in CAD. Genomic variants of TNF‐β may therefore contribute to the complex susceptibility for the metabolic syndrome in patients with CAD.