Title : Chronic heavy alcohol consumption influences the association between genetic variants of GCK or INSR and the development of diabetes in men: A 12-year follow-up study.

Pub. Date : 2019 Dec 27

PMID : 31882596






7 Functional Relationships(s)
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1 Chronic heavy alcohol consumption influences the association between genetic variants of GCK or INSR and the development of diabetes in men: A 12-year follow-up study. Alcohols glucokinase Homo sapiens
2 We aimed to determine whether the longitudinal associations between genetic variants of glucokinase (GCK) and insulin receptor (INSR) and the risk of developing diabetes were influenced by chronic heavy alcohol consumption. Alcohols glucokinase Homo sapiens
3 We aimed to determine whether the longitudinal associations between genetic variants of glucokinase (GCK) and insulin receptor (INSR) and the risk of developing diabetes were influenced by chronic heavy alcohol consumption. Alcohols glucokinase Homo sapiens
4 We identified that these GCK and INSR polymorphisms are affected by chronic heavy alcohol consumption and have an effect on the incidence of diabetes. Alcohols glucokinase Homo sapiens
5 The incidence of diabetes was increased in chronic heavy alcohol drinkers carrying the C allele of GCK compared with never-drinkers with the C allele (HR, 2.15; 95% CI 1.30-3.57), and was increased in chronic heavy alcohol drinkers who were not carrying the INSR haplotype (-/-) compared with never-drinkers carrying the AACT haplotype (HR, 1.98; 95% CI 1.24-3.18). Alcohols glucokinase Homo sapiens
6 The incidence of diabetes was increased in chronic heavy alcohol drinkers carrying the C allele of GCK compared with never-drinkers with the C allele (HR, 2.15; 95% CI 1.30-3.57), and was increased in chronic heavy alcohol drinkers who were not carrying the INSR haplotype (-/-) compared with never-drinkers carrying the AACT haplotype (HR, 1.98; 95% CI 1.24-3.18). Alcohols glucokinase Homo sapiens
7 These results potentially suggest that chronic heavy alcohol consumption induce beta-cell dysfunction partially mediated by decreased GCK expression or decline of insulin sensitivity via inhibition of INSR, thereby contributing to the development of diabetes. Alcohols glucokinase Homo sapiens