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Abstract
BackgroundAlterations in extracellular vesicles (EVs), including exosomes and microparticles, contribute to cardiovascular disease. We hypothesized that obesity could favour enhanced release of EVs from adipose tissue, and thereby contribute to cardiovascular risk via obesity-induced metabolic complications. The objectives of this study were: 1) to investigate the relation between the quantity, distribution and (dys) function of adipose tissue and plasma concentrations of atherothrombotic EV-markers; 2) to determine the relation between these EV-markers and the prevalence of the metabolic syndrome; and 3) to assess the contribution of EV markers to the risk of incident type 2 diabetes.MethodsIn 1012 patients with clinically manifest vascular disease, subcutaneous and visceral fat thickness was measured ultrasonographically. Plasma EVs were isolated and levels of cystatin C, serpin G1, serpin F2 and CD14 were measured, as well as fasting metabolic parameters, hsCRP and adiponectin. The association between adiposity, EV-markers, and metabolic syndrome was tested by multivariable linear and logistic regression analyses. As sex influences body fat distribution, sex-stratified analyses between adipose tissue distribution and EV-markers were performed. The relation between EV-markers and type 2 diabetes was assessed with Cox regression analyses.ResultsHigher levels of hsCRP (β 5.59; 95% CI 3.00–8.18) and lower HDL-cholesterol levels (β-11.26; 95% CI −18.39 – -4.13) were related to increased EV-cystatin C levels, and EV-cystatin C levels were associated with a 57% higher odds of having the metabolic syndrome (OR 1.57; 95% CI 1.19–2.27). HDL-cholesterol levels were positively related to EV-CD14 levels (β 5.04; 95% CI 0.07–10.0), and EV-CD14 levels were associated with a relative risk reduction of 16% for development of type 2 diabetes (HR 0.84, 95% CI 0.75–0.94), during a median follow up of 6.5 years in which 42 patients developed type 2 diabetes.ConclusionsIn patients with clinically manifest vascular disease, EV-cystatin C levels were positively related, and EV-CD14 levels were negatively related to metabolic complications of obesity.
Highlights
Alterations in extracellular vesicles (EVs), including exosomes and microparticles, contribute to cardiovascular disease
Mean visceral AT (VAT) thickness and Waist circumference (WC) were higher in males than females (VAT males: 9.9 ± 2.6 cm, females: 8.3 ± 2.4 cm, WC males: 97 ± 10 cm, females: 88 ± 12 cm), and mean subcutaneous AT (SAT) thickness was higher in females than in males. 51% of the patients had metabolic syndrome, defined by the Adult Treatment Panel (ATP) III criteria [10], of which 36% had central obesity, 94% were hypertensive, 39% had hypertriglyceridemia, 29% had low HDL-cholesterol levels and 63% had an impaired fasting glucose
EV-serpin F2 levels were lower in patients with more subcutaneous fat (36.81 pg/μg versus 37.37 pg/μg, p = 0.002) and higher in patients suffering from hyperlipidaemia compared to patients without hyperlipidaemia (40.16 pg/μg versus 35.44 pg/μg, p = 0.013)
Summary
Alterations in extracellular vesicles (EVs), including exosomes and microparticles, contribute to cardiovascular disease. Obese individuals are at increased risk of developing cardiovascular disease (CVD), a consequence of adipose tissue (AT) expansion and subsequent dysfunction [1,2]. Expression of the anti-inflammatory adipokine adiponectin is downregulated in adipocytes [8] This inflammatory milieu leads to metabolic complications that predispose to the development of CVD, including lowgrade systemic inflammation, insulin resistance [9] and development of the metabolic syndrome and type 2 diabetes [10,11]. Further emphasizing the link between VAT and CVD are sex differences in body fat distribution, where males are both prone to develop abdominal obesity due to accumulation of visceral fat and suffer from a higher incidence of metabolic and cardiovascular disease [12]
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