The effect of dietary salt load on insulin resistance in hypertensive patients with the Gly972Arg polymorphism of the insulin receptor substrate 1 (IRS-1) gene

Abstract

Background This work was designed to assess the effect of various dietary salt loads on the frequency of insulin resistance in hypertensive patients with Gly972Arg polymorphism of the IRS-1 gene.
Material and methods The study group comprised 115 non-obese patients aged 27.48 ± 5.15 years with essential uncomplicated arterial hypertension. Gly972Arg polymorphism of the IRS-1 gene was disclosed according to Yamada. The patients were hospitalized and placed on 7-day cycles of normal-, low- and high-sodium diet. Blood was sampled on day 7 of the normal sodium diet for the measurement of insulin, plasma renin activity, and aldosterone. Blood was again sampled on day 7 of the low- and high-sodium diet for the same determinations. In addition, 24 h ABPM was carried out on day 6 of the low- and high-sodium diet cycle. Insulin resistance was assessed with HOMA.
Results The GA genotype was revealed in 16 patients (13.9%). This genotype polymorphism of the IRS-1 gene was associated with higher frequency of insulin resistance, particularly on a normal and high-sodium diet. On low-sodium diet insulin resistance was less frequent in GA patients but still remained significantly more frequent than in GG patients. Higher concentrations of total cholesterol, LDL-cholesterol, and triglycerides and lower concentrations of HDL-cholesterol were demonstrated in GA patients. Significant increase in insulin concentrations and HOMA during the high-sodium cycle were observed in GA patients only. In the case of the remaining parameters, changes induced by varying sodium load were similar in GA and GG patients.
Conclusions 1. Hypertensive patients with the GA genotype Gly972Arg polymorphism of the IRS-1 gene are predisposed to insulin resistance and disorders of lipid metabolism. 2. High-sodium diet enhances insulin resistance in patients with the GA genotype suggesting early progression to cardiovascular pathology if the patient remains hypertensive and salt consumption is not reduced.