ADPKD protects against diabetogenic effects associated with genetically-predicted lactase persistence.

Abstract

IntroductionThe LCT: -13910C>T (rs4988235) polymorphism is associated with lactase persistence. Our previous study revealed impairment of pancreatic beta-cell function after an oral glucose tolerance test (OGTT) without a significant decrease in insulin sensitivity in ADPKD patients. The aim of the present study was to analyse clinical and biochemical parameters including indices of insulin sensitivity in regard to LCT polymorphism both in ADPKD patients and controls.Material and methodsThe study group consisted of 49 ADPKD patients and the control group comprised 50 healthy subjects. Plasma glucose, insulin and C-peptide concentrations were measured during WHO OGTT. The LCT polymorphism was identified by PCR-RFLP assay of samples of genomic DNA extracted from peripheral blood leukocytes.ResultsIn the ADPKD group no significant differences in clinical and biochemical parameters were found between patients with lactase non-persistence (LNP) and individuals with lactase persistence (LP). In healthy subjects with LP (LCT: CT or TT genotype) body fat, the levels of insulin, C-peptide and insulin/glucose ratio (at OGTT times 0 and 120 minutes); area under curve ratios of secretory 1st and 2nd phase, homeostasis model assessment (HOMA)-insulin resistance and % beta, were significantly higher as compared with CC homozygotes (LNP). In addition, HOMA% sensitivity and indices of insulin sensitivity in LP controls were significantly lower as compared with healthy subjects with LNP.ConclusionsOur results suggest that ADPKD patients are protected against a lactase-persistence-associated diabetogenic increase in insulin resistance.