Abstract

The aim of our study was to assess the impact of whole blood lead (Pb-B) levels on changes in peripheral blood morphology and selected biochemical parameters, and the severity of depression in peri-menopausal women at risk of metabolic syndrome (pre-MetS) or with metabolic syndrome (MetS). The study involved 233 women from the general population of the West Pomeranian Province (Poland) aged 44–65 years. The intensity of menopausal symptoms and the severity of depression was examined using the Blatt–Kupperman Index (KI) and the Beck Depression Inventory (BDI). C-reactive protein (CRP), insulin, glucose, glycated hemoglobin (HbA1C), high-density lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol, triglyceride levels (TG), cortisol, morphology of blood cells and homeostasis model assessment for insulin resistance (HOMA-IR) and Pb-B was measured. Women with MetS had higher levels of glucose, HbA1C, HDL, LDL, TG, cortisol, insulin and higher HOMA-IR. No significant differences in Pb-B were observed between pre-MetS and the control group, and between pre-MetS and the MetS group. A significant correlation was noticed between Pb-B vs. the percentage of monocytes in blood, and blood cortisol levels in women with MetS; Pb-B vs. lymphocyte count and HbA1C in the pre-MetS group, as well as in the BDI scores between the MetS and pre-MetS group. We cannot clearly state that exposure to Pb is an environmental factor that can be considered as a risk factor for MetS in this studied group.

Highlights

  • Metabolic syndrome (MetS) involves the coexistence of metabolic risk factors that are linked to one another

  • Status confirmed that women with metabolic syndrome (MetS) had higher mean levels of glucose, triglyceride levels (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), HbA1C, cortisol, insulin, and higher homeostasis model assessment for insulin resistance (HOMA-IR), which is in line with the definition of MetS (Table 2)

  • This heavy metal triggers oxidative stress through binding to sulfhydryl groups of proteins, causing inactivation of numerous enzymatic reactions and amino acids, and depletion of antioxidants [61,62]. These mechanisms can lead to the development of cardiovascular disease, diabetes, atherosclerosis, neurological disorders, and chronic inflammation [61]

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Summary

Introduction

Metabolic syndrome (MetS) involves the coexistence of metabolic risk factors that are linked to one another. They include visceral obesity, atherogenic dyslipidemia in the form of hypertriglyceridemia and decreased HDL cholesterol levels, carbohydrate metabolism disorders (impaired fasting glycemia), carbohydrate intolerance, type 2 diabetes, and hypertension [1]. Metabolic risk factors, included in the above sets of MetS criteria, contribute to the development of atherosclerotic cardiovascular disease [3], type 2 diabetes (if it is not a component of MetS) [4], and neurological disorders [5], and they raise both overall and cardiovascular mortality rate [6,7]. The results of epidemiological research indicate that MetS is widely spread both across the US [9,10,11], and Europe [12,13,14], including Poland [15,16]

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