Abstract

Introduction. The high incidence of arterial hypertension (AH) in the population, its close association with menopause and disorders of carbohydrate metabolism with an emphasis on the predictive role of fasting glycemia (FG) for type 2 diabetes mellitus draws attention to the phenotype of the formation of metabolic syndrome (MS) in perimenopause depending on the presence of hypertension without dysglycemia. Aim of the research. To evaluate the associations between blood pressure (BP) levels and FG during the formation of insulin resistant menopausal MS in a cohort of normoglycemic women aged 35–59 years with AH and normotensive. Materials and methods. In the perimenopausal cohort of women aged 35–59 years without dysglycemia (n = 88), 58 women had hypertension, 30 were normotensive. The following were determined: body mass index (BMI), waist circumference (WC), levels of BP, triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), insulin, follicle-stimulating hormone (FSH) and estradiol, FG, TyG and HOMA2 family (HOMA2-IR and HOMA2-%B) indices. Using SPSS (version 17), we estimated the median (25; 75%); intergroup differences according to the Mann-Whitney test; then, the correlation analyses were carried out: according to Spearman (R) and partial (Rpc) to level the influence of age. Results. Significant associations of systolic BP (SBP) and FG levels, direct and mediated through lipid (TG and HDL-C) and anthropometric (WC) parameters of MS, were revealed with most of the correlations being only partially age-dependent. Among these parameters, the mediators of insulin resistance, the associations of SBP and FG with WC are the most pronounced; it is WC that stably correlates with insulin resistance indices, more specifically with TyG. The correlations of TG levels with HDL-C (R = –0.564; p < 0.001) are also relevant when the influence of age is leveled (Rpc = –0.477; p < 0.001); with them, as well as with the levels of insulin and the duration of postmenopause, FG correlates. BP levels, especially systolic, form correlations with insulin resistance indices, more stable with non-insulin TyG index, in contrast to age-dependent relationships with HOMA2-IR. Conclusion. The extensiveness of the revealed correlations between BP and FG levels with markers and factors for the formation of menopausal MS, including the relation of BP with HOMA2-IR indices and especially TyG, reflects its insulin resistant pathogenetic basis. Along with this, significant stable correlations of the duration of postmenopause with FG reflect a high risk of progression to dysglycemia in the analyzed phenotype of metabolic syndrome and allow us to consider menopause as a unique factor contributing to the rapid clustering of MS in women, determining the interest in clarifying its formation trajectories.

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