Bioavailable testosterone is independently associated with Fatty Liver Index in postmenopausal women

Abstract

IntroductionPrevious studies have examined the correlation between hyperandrogenemia and non-alcoholic fatty liver disease (NAFLD) in women and showed contradictory results. Therefore, we aimed to evaluate the relationship between testosterone level and Fatty Liver Index (FLI), as a surrogate marker for NAFLD, in a cohort of postmenopausal women.Material and methodsA total of 150 postmenopausal women were included in this cross-sectional study. Anthropometric and biochemical parameters, as well as blood pressure, were obtained. Non-alcoholic fatty liver disease is assessed by FLI, an algorithm based on body mass index, waist circumference, triglycerides and γ-glutamyl transferase, as a simple and accurate predictor of hepatic steatosis. Women were divided into three groups (FLI < 30, n = 80; 30 ≤ FLI < 60, n = 44; FLI ≥ 60, n = 26). Homeostasis model assessment of insulin resistance (HOMA-IR) as a surrogate marker of insulin resistance was calculated.ResultsMultiple linear regression analysis revealed that the best model consisted of 4 parameters (e.g., bioavailable testosterone (β = 0.288, p = 0.001), log HOMA-IR (β = 0.227, p = 0.005), log high-sensitivity C-reactive protein (β = 0.322, p < 0.001), and retinol-binding protein 4 (β = 0.226, p < 0.001)). Adjusted R2 for the best model was 0.550, which means that as much as 55.0% of variation in FLI could be explained with this model.ConclusionsBioavailable testosterone is independently associated with FLI in postmenopausal women.

Body mass index and insulin resistance as independent predictors of hypertension in postmenopausal women

“…Increased visceral fat mass is a source of proinflammatory adipocytokines [5][6][7][8], exerting a low-grade inflammation environment which could predispose to the future hypertension occurrence [9]. In addition, increased abdominal fat mass is accompanied with increased insulin resistance [4,8]. However, even though previous studies confirmed the association between obesity and hypertension, the underlying pathophysiological mechanism is not well elucidated [10,11].…”

“…The current cross-sectional study derived from our previous works investigating the utility of examining cardiometabolic markers in postmenopausal women [1][2][3][4][5][6][7]. A total of 150 postmenopausal women nontreated with medications (among them 44.7% hypertensive) were included in cross-sectional study.…”

“…The investigation was carried out in compliance with the Declaration of Helsinki, and Ethical Committee of Primary Health Care Center in Podgorica, Montenegro approved the study protocol. Anthropometric measurements Basic anthropometric measurements were obtained, as described previously [4]. Biochemical analyses Biochemical parameters were measured as described elsewhere [4].…”

“…Anthropometric measurements Basic anthropometric measurements were obtained, as described previously [4]. Biochemical analyses Biochemical parameters were measured as described elsewhere [4]. Serum levels of glucose, lipid parameters [e.g., total cholesterol (TC), high density lipoprotein cholesterol (HDL-c), low density lipoprotein cholesterol (LDL-c), triglycerides (TG)], bilirubin, uric acid,creatinine, as well as the activity of aspartat aminotransferase (AST), alanine aminotransferase (ALT) and gamma-glutamyl transferase (GGT), were measured spectrophotometrically (Roche Cobas 400, Mannheim, Germany).…”

“…Therefore, it is not surprising that postmenopausal women had higher incidence of cardiometabolic disorders than premenopausal women [1,3]. It is speculated that redistribution of adipose tissue towards visceral region, due to hormonal changes may be the main pathogenic entity, consequently leading to increased cardiometabolic risk [4] in postmenopause. Increased visceral fat mass is a source of proinflammatory adipocytokines [5][6][7][8], exerting a low-grade inflammation environment which could predispose to the future hypertension occurrence [9].…”