Association of free testosterone and sex hormone binding globulin with metabolic syndrome and subclinical atherosclerosis but not blood pressure in hypertensive perimenopausal women

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Abstract

Introduction

Data on the role of androgens as potential mediators of increasing cardiovascular risk in women at midlife are controversial. The aim of the study was to analyze the relationship of free testosterone (FT) and sex hormone binding globulin (SHBG) with blood pressure and subclinical organ damage and metabolic syndrome (MS) in middle aged hypertensive women.

Material and methods

One hundred and fifty-two women with newly diagnosed arterial hypertension were included in the study. In all subjects blood pressure measurements were performed as well as echocardiographic examination with left ventricular structure and function assessment (GE Vivid 7.0), carotid ultrasound with measurement of intima-media thickness (IMT), and carotid-femoral pulse wave velocity (PWV) measurement (Sphygmocor). A fasting blood sample was taken to measure glucose and lipid concentrations. Serum testosterone and SHBG were measured. Free testosterone was calculated according to the Vermeulen formula. Metabolic syndrome was defined following the International Diabetes Federation (IDF) recommendations.

Results

Free testosterone was significantly higher and SHBG lower in women with MS independently of menopausal status. The odds ratio of MS per quartile increment in FT after adjustment for covariates was 2.06 (95% CI: 1.16–3.65). There was no correlation between FT, SHBG and blood pressure. Free testosterone was associated with decreased left ventricular diastolic function (E/A ratio β = –0.19, p = 0.05) and subclinical atherosclerosis (IMT β = 0.34, p = 0.009), but not arterial stiffness.

Conclusions

Free testosterone and SHBG independently of menopause status are related to MS. Free testosterone is associated with worse metabolic profile, subclinical atherosclerosis and impaired diastolic function of the left ventricle.

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Most cited references 35

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Relation of BMI and physical activity to sex hormones in postmenopausal women.

Anne McTiernan, LieLing Wu, Chu Chin Chen … (2006)

Levels of estrogen, androgen, and prolactin have been related to risk of postmenopausal breast cancer. However, the determinants of these hormone concentrations are not established. The purpose of this study was to examine correlates of endogenous sex hormones. Associations among adiposity, physical activity, and diet and concentrations of estradiol, free estradiol, estrone, testosterone, free testosterone, sex hormone-binding globulin (SHBG), androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate, and prolactin were evaluated in 267 postmenopausal women randomly selected from the Women's Health Initiative Dietary Modification Trial. In multiple regression analyses on log-transformed hormones, BMI was positively associated with estrone (beta = 0.031, p < 0.001), estradiol (beta = 0.048, p < 0.001), free estradiol (beta = 0.062, p < 0.001), free testosterone (beta = 0.017, p = 0.02), and prolactin (beta = 0.012, p = 0.02) and negatively associated with SHBG (beta = -0.02, p = 0.001). Total physical activity (metabolic equivalent tasks per week) was negatively associated with concentrations of estrone, estradiol, and androstenedione (beta = -0.006, -0.007, and -0.005, respectively, all p < or = 0.05). Using a composite variable of BMI and physical activity dichotomized by median values, women with high BMI/low physical activity had a mean estrone concentration of 28.8 pg/mL, compared with 24.1, 19.9, and 18.4 pg/mL for women with high BMI/high physical activity, low BMI/low physical activity, and low BMI/high physical activity, respectively (p trend < 0.001). Similar trends were observed for estradiol and free estradiol and, in inverse, for SHBG. These associations may, in part, explain the positive associations between overweight/obesity and a sedentary lifestyle on breast cancer risk.

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Testosterone relaxes rabbit coronary arteries and aorta.

Rebecca C. Beale, Jennifer J. P. Collins, Julie Wilson … (1995)

Until menopause, women appear to be protected from coronary heart disease. Evidence suggests that estrogen may play a role in the protection of the cardiovascular system by exerting a beneficial effect on risk factors such as cholesterol metabolism and by a direct effect on the coronary arteries. To date there has been no evidence linking testosterone with the occurrence of coronary heart disease. Testosterone may affect the cardiovascular system directly, thus partially explaining the difference in the incidence of coronary artery disease in men and premenopausal women. The purpose of this study was to assess the direct effect of testosterone and a number of testosterone analogues on rabbit coronary arteries and aorta in vitro. Rings of coronary artery and aorta of adult male or nonpregnant female New Zealand White rabbits were suspended in organ baths containing Krebs solution; isometric tension then was measured. The response to testosterone was investigated in prostaglandin F2 alpha (PGF 2 alpha)- and KCl-contracted rings. The effects of endothelium and nitric oxide synthase, prostaglandin synthetase, and guanylate cyclase inhibition on testosterone-induced relaxation were investigated. The effects of ATP-sensitive potassium channels and potassium conductance were also assessed. Relaxing responses in the presence of aromatase inhibition and testosterone receptor blockade were performed. The relaxing responses to the testosterone analogues etiocholan-3 beta-ol-17-one, epiandrosterone, 17 beta-hydroxy-5 alpha-androst-1-en-3-one, androst-16-en-3-ol, and testosterone enanthanate were measured. Testosterone relaxed rabbit coronary arteries and aorta. There was no significant difference between the relaxation effect of testosterone with or without endothelium. Similar results were obtained from male and nonpregnant female rabbits. The relaxing response of testosterone in the coronary artery was significantly greater than in the aorta. The relaxing response of testosterone in the coronary artery was significantly reduced by the potassium channel inhibitor barium chloride but not by the ATP-sensitive potassium channel inhibitor glibenclamide. The relaxing response to testosterone was greater in PGF 2 alpha-contracted rings compared with KCl-contracted rings. Inhibitors of nitric oxide synthase, prostaglandin synthetase, and guanylate cyclase did not affect relaxation induced by testosterone. Inhibition of aromatase and testosterone receptors did not affect relaxation. Testosterone did not shift the rabbit coronary arterial calcium concentration-dependent contraction curves, whereas verapamil did. There were, however, significant differences in the relaxing response to testosterone compared with testosterone analogues. Testosterone was the most potent relaxing agent, suggesting that there may be a structure-function relation in the relaxing response. Testosterone induces endothelium-independent relaxation in isolated rabbit coronary artery and aorta, which is neither mediated by prostaglandin I2 or cyclic GMP. Potassium conductance and potassium channels but not ATP-sensitive potassium channels may be involved partially in the mechanism of testosterone-induced relaxation. The in vitro relaxation is independent of sex and of a classic receptor. The coronary artery is significantly more sensitive to relaxation by testosterone than the aorta. Testosterone is a more potent relaxing agent of rabbit coronary artery than other testosterone analogues.

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Androgen generation in adipose tissue in women with simple obesity--a site-specific role for 17beta-hydroxysteroid dehydrogenase type 5.

Iwona Bujalska, Christine Stewart, Wiebke Arlt … (2004)

Women with polycystic ovary syndrome (PCOS) have high circulating androgens, thought to originate from ovaries and adrenals, and frequently suffer from the metabolic syndrome including obesity. However, serum androgens are positively associated with body mass index (BMI) not only in PCOS, but also in simple obesity, suggesting androgen synthesis within adipose tissue. Thus we investigated androgen generation in human adipose tissue, including expression of 17beta-hydroxysteroid dehydrogenase (17beta-HSD) isozymes, important regulators of sex steroid metabolism. Paired omental and subcutaneous fat biopsies were obtained from 27 healthy women undergoing elective abdominal surgery (age range 30-50 years; BMI 19.7-39.2 kg/m(2)). Enzymatic activity assays in preadipocyte proliferation cultures revealed effcient conversion of androstenedione to testosterone in both subcutaneous and omental fat. RT-PCR of whole fat and preadipocytes of subcutaneous and omental origin showed expression of 17beta-HSD types 4 and 5, but no relevant expression of 17beta-HSD types 1, 2, or 3. Microarray analysis confirmed this expression pattern (17beta-HSD5>17beta-HSD4) and suggested a higher expression of 17beta-HSD5 in subcutaneous fat. Accordingly, quantitative real-time RT-PCR showed significantly higher expression of 17beta-HSD5 in subcutaneous compared with omental fat (P<0.05). 17beta-HSD5 expression in subcutaneous, but not omental, whole fat correlated significantly with BMI (r=0.51, P<0.05). In keeping with these findings, 17beta-HSD5 expression in subcutaneous fat biopsies from six women taking part in a weight loss study decreased significantly with weight loss (P<0.05). A role for 17beta-HSD5 in adipocyte differentiation was further supported by the observed increase in 17beta-HSD5 expression upon differentiation of stromal preadipocytes to mature adipocytes (n=5; P<0.005), which again was higher in cells of subcutaneous origin. Functional activity of 17beta-HSD5 also significantly increased with differentiation, revealing a net gain in androgen activation (androstenedione to testosterone) in subcutaneous cultures, contrasting with a net gain in androgen inactivation (testosterone to androstenedione) in omental cultures. Thus, human adipose tissue is capable of active androgen synthesis catalysed by 17beta-HSD5, and increased expression in obesity may contribute to circulating androgen excess.

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Author and article information

Journal

Journal ID (nlm-ta): Arch Med Sci

Journal ID (iso-abbrev): Arch Med Sci

Journal ID (publisher-id): AMS

Title: Archives of Medical Science : AMS

Publisher: Termedia Publishing House

ISSN (Print): 1734-1922

ISSN (Electronic): 1896-9151

Publication date (Electronic): 18 May 2016

Publication date (Print): 01 June 2016

Volume: 12

Issue: 3

Pages: 521-528

Affiliations

First Department of Cardiology, Interventional Electrocardiology and Hypertension, Jagiellonian University Medical College, Krakow, Poland

Author notes

Corresponding author: Agnieszka Olszanecka, First Department of Cardiology, Interventional Electrocardiology and Hypertension, Jagiellonian University Medical College, 17 Kopernika St, 31-501 Krakow, Poland. Phone: +48 12 424 73 00, Fax: + 48 12 424 73 20. E-mail: olszanec@ 123456su.krakow.pl

Article

Publisher ID: 27566

DOI: 10.5114/aoms.2016.59925

PMC ID: 4889686

PubMed ID: 27279843

SO-VID: a1f3d054-62b1-4b43-990c-23b7eb5b5e15

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.

Association of free testosterone and sex hormone binding globulin with metabolic syndrome and subclinical atherosclerosis but not blood pressure in hypertensive perimenopausal women

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Abstract

Introduction

Material and methods

Results

Conclusions

Related collections

Karger: Nutrition and Dietetics

Most cited references 35

Relation of BMI and physical activity to sex hormones in postmenopausal women.

Testosterone relaxes rabbit coronary arteries and aorta.

Androgen generation in adipose tissue in women with simple obesity--a site-specific role for 17beta-hydroxysteroid dehydrogenase type 5.

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