Endothelial dysfunction in hyperandrogenic polycystic ovary syndrome is not explained by either obesity or ectopic fat deposition

Sprung, Victoria S.; Jones, Helen; Pugh, Christopher J. A.; Aziz, Nabil; Daousi, Christina; Kemp, Graham J.; Green, Daniel; Cable, N. Timothy; Cuthbertson, Daniel J.

doi:10.1042/cs20130186

Cited by 35 publications

(25 citation statements)

References 43 publications

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“…Based on previously reported data (14,30), an absolute mean difference of Ն3.4% with a common standard deviation of 2.6% represents clinically relevant differences between groups. For the trial intervention, previously reported data (14,29) indicate that an absolute mean difference of Ն3.6% with a common standard deviation of 3.4% represents a clinically relevant improvement.…”

Section: Discussionmentioning

confidence: 99%

Exercise training reverses endothelial dysfunction in nonalcoholic fatty liver disease

Pugh

Sprung

Kemp

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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107

120

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fatty liver disease (NAFLD) is an independent risk factor for cardiovascular disease (CVD). Endothelial dysfunction is an early manifestation of atherosclerosis and an important prognostic marker for future cardiovascular events. The aim of this study was twofold: to examine 1) the association between liver fat, visceral adipose tissue (VAT), and endothelial dysfunction in obese NAFLD patients and 2) the impact of supervised exercise training on this vascular defect. Brachial artery endothelial function was assessed by flow-mediated dilatation (FMD) in 34 obese NAFLD patients and 20 obese controls of similar age and cardiorespiratory fitness [peak oxygen uptake (V O2 peak)] (48 Ϯ 2 vs. 47 Ϯ 2 yr; 27 Ϯ 1 vs. 26 Ϯ 2 ml·kg Ϫ1 ·min Ϫ1Ϫ1 ). Magnetic resonance imaging and spectroscopy quantified abdominal and liver fat, respectively. Twenty-one NAFLD patients completed either 16 wk of supervised moderate-intensity exercise training (n ϭ 13) or conventional care (n ϭ 8). Differences between NAFLD and controls were compared using independent t-tests and effects of interventions by analysis of covariance. NAFLD patients had higher liver fat [11.6% (95% CI ϭ 7.4, 18.1), P Ͻ 0.0005] and VAT [1.6 liters (95% CI ϭ 1.2, 2.0), P Ͻ 0.0001] than controls and exhibited impaired FMD compared with controls [Ϫ3.6% (95% CI ϭ Ϫ4.9, Ϫ2.2), P Ͻ 0.0001]. FMD was inversely correlated with VAT (r ϭ Ϫ0.54, P ϭ 0.001) in NAFLD, although the impairment in FMD remained following covariate adjustment for VAT [3.1% (95% CI ϭ 1.8, 4.5), P Ͻ 0.001]. Exercise training, but not conventional care, significantly improved V O2 peak [9.1 ml·kg Ϫ1 ·min Ϫ1 (95% CI ϭ 4.1, 14.1); P ϭ 0.001] and FMD [3.6% (95% CI ϭ 1.6, 5.7), P ϭ 0.002]. Endothelial dysfunction in NAFLD cannot be fully explained by excess VAT but can be reversed with exercise training; this has potential implications for the primary prevention of CVD in NAFLD. nonalcoholic fatty liver disease; flow-mediated dilation; cardiovascular risk; exercise training NONALCOHOLIC FATTY LIVER DISEASE (NAFLD) is a disease spectrum ranging from simple steatosis, progressing to necroinflammatory changes (nonalcoholic steatohepatitis) and in a subset, to cirrhosis, fibrosis, and end-stage liver disease (20). NAFLD is the most common form of chronic liver disease in Western society, affecting 20 -30% of the general population (6) and up to ϳ60% of individuals with type 2 diabetes mellitus (43). NAFLD is regarded as the hepatic manifestation of the metabolic syndrome, coexisting with multiple cardiometabolic risk factors, including obesity, insulin resistance, hypertension, and dyslipidemia (34).NAFLD increases the risk of chronic liver disease, yet epidemiological studies suggest that cardiovascular disease (CVD) accounts for more deaths in NAFLD than liver disease, some reporting CVD to be the leading cause of mortality (10,23,34). Indeed, there is strong evidence that NAFLD patients are at greater risk of CVD than controls and that NAFLD is an independent predictor of cardiovascular morbidity and mortality ...

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Section: Discussionmentioning

confidence: 99%

Exercise training reverses endothelial dysfunction in nonalcoholic fatty liver disease

Pugh

Sprung

Kemp

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

107

120

View full text Add to dashboard Cite

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“…Endothelial dysfunction is a key early step in the development of atherosclerosis (Celermajer et al 1992). It was well documented that endothelial dysfunction exists in subjects with PCOS (Lambert et al 2015, Srung et al 2014. Moreover, some studies have shown that endothelial dysfunction is partially dependent on inflammation and oxidative stress in PCOS (Pertynska-Vol.…”

Section: Introductionmentioning

confidence: 99%

Serum HMGB1 Levels and Its Association With Endothelial Dysfunction in Patients With Polycystic Ovary Syndrome

Wang

Lin²,

Xiang³

2018

Physiol Res

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High-mobility group box 1 (HMGB1) is newly discovered protein, which play a crucial role in the pathogenesis of systemic inflammation. Recent studies showed that HMGB1 is one of the important pathophysiological mechanisms in the occurrence and development of atherosclerosis. The purpose of the present study was to investigate the relationship between serum HMGB1 levels and endothelial function in patients with polycystic ovary syndrome (PCOS). Eighty newly diagnosed patients with PCOS and eighty normal women of similar age were selected. Metformin treatment (1,500 mg/day) was initiated in all patients for a period of consecutive 3 months. Serum HMGB1 levels were measured by ELISA. High resolution ultrasound was used to measure the brachial artery diameter at rest, after reactive hyperemia (flow-mediated arterial dilation, FMD) and after sublingual glyceryltrinitrate. Serum HMGB1 levels in PCOS were 24.87±14.93 ng/ml, which were significantly higher than that in controls (8.82±3.55 ng/ml, p<0.01). After 3 months treatment, serum HMGB1 levels decreased significantly (p<0.05). By dividing the distribution of HMGB1 levels into quartiles, serum HMGB1 levels were increased gradually with the increase of testosterone levels (p<0.05), whereas the FMD levels decreased (p<0.05). Multiple stepwise linear regression analysis showed that FMD (estimated coefficient β=-0.69, p=0.005), testosterone (β=0.31, p=0.045), TBARS (β=0.69, p=0.012) and hs-CRP levels (β=0.68, p=0.001) were significantly associated with HMGB1. The absolute changes in HMGB1 showed a positive correlation with the changes in testosterone (p<0.05) and negative correlation with the changes in FMD (p<0.05) in patients with PCOS during the course of metformin therapy. Serum HMGB1 levels are correlated with endothelial dysfunction in patients with PCOS. Our study suggests that HMGB1 may contribute to the early stage of atherosclerosis in patients with PCOS

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“…; Sprung et al . ), and it has been reported that genetic female‐to‐male transsexuals taking high‐dose androgens exhibit impaired vascular smooth muscle reactivity (McCredie et al . ).…”

Section: Introductionmentioning

confidence: 99%

Sex differences in vascular endothelial function and health in humans: impacts of exercise

Green

Hopkins

Jones

et al. 2016

Experimental Physiology

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New Findings r What is the topic of this review?This brief review discusses potential sex differences in arterial function across the age span, with special emphasis on the effects of oestrogen and testosterone on the vascular endothelium. r What advances does it highlight?We discuss the relationship between the impacts of sex hormones on arterial function and health in the context of epidemiological evidence pertaining to the menopause and ageing. Studies performed in humans are emphasized, alongside insights from animal studies. Findings suggest that the combination of exercise and hormone administration should be potentially synergistic or additive in humans.This brief review presents historical evidence for the purported impacts of male and female sex hormones on the vasculature in humans, including effects on macro-and microvascular function and health. Impacts of ageing on hormonal changes and arterial function are considered in the context of the menopause. Physiological data are presented alongside clinical outcomes from large trials, in an attempt to rationalize disparate findings along the bench-to-bedside continuum. Finally, the theoretical likelihood that exercise and hormone treatment may induce synergistic and/or additive vascular adaptations is developed in the context of recent laboratory studies that have compared male and female responses to training. Differences between men and women in terms of the impact of age and cardiorespiratory fitness on endothelial function are addressed. Ultimately, this review highlights the paucity of high-quality and compelling evidence regarding the fundamental impact, in humans, of sex differences on arterial function and the moderating impacts of exercise on arterial function, adaptation and health at different ages in either sex.

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Endothelial dysfunction in hyperandrogenic polycystic ovary syndrome is not explained by either obesity or ectopic fat deposition

Cited by 35 publications

References 43 publications

Exercise training reverses endothelial dysfunction in nonalcoholic fatty liver disease

Exercise training reverses endothelial dysfunction in nonalcoholic fatty liver disease

Serum HMGB1 Levels and Its Association With Endothelial Dysfunction in Patients With Polycystic Ovary Syndrome

Sex differences in vascular endothelial function and health in humans: impacts of exercise

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