Abstract
Obesity is defined as excessive body fat accumulation, and worldwide obesity has nearly tripled since 1975. Excess of free fatty acids (FFAs) and triglycerides in obese individuals promote ectopic lipid accumulation in the liver, skeletal muscle tissue, and heart, among others, inducing insulin resistance, hypertension, metabolic syndrome, type 2 diabetes (T2D), atherosclerosis, and cardiovascular disease (CVD). These diseases are promoted by visceral white adipocyte tissue (WAT) dysfunction through an increase in pro-inflammatory adipokines, oxidative stress, activation of the renin-angiotensin-aldosterone system (RAAS), and adverse changes in the gut microbiome. In the heart, obesity and T2D induce changes in substrate utilization, tissue metabolism, oxidative stress, and inflammation, leading to myocardial fibrosis and ultimately cardiac dysfunction. Peroxisome proliferator-activated receptors (PPARs) are involved in the regulation of carbohydrate and lipid metabolism, also improve insulin sensitivity, triglyceride levels, inflammation, and oxidative stress. The purpose of this review is to provide an update on the molecular mechanisms involved in obesity-linked CVD pathophysiology, considering pro-inflammatory cytokines, adipokines, and hormones, as well as the role of oxidative stress, inflammation, and PPARs. In addition, cell lines and animal models, biomarkers, gut microbiota dysbiosis, epigenetic modifications, and current therapeutic treatments in CVD associated with obesity are outlined in this paper.
Highlights
The obesity epidemic has spread globally in the past four decades
Troseid et al [114] described the association of trimethylamine N-oxide (TMAO) with disease severity and survival of patients with chronic heart failure (HF); the results showed an elevated plasma level of TMAO in patients (n = 155) with chronic HF compared with the control group
We have described the pathophysiologic mechanisms involved in obesity-related cardiovascular disease (CVD), as well as the role of Peroxisome proliferator-activated receptors (PPARs), epigenetic modifications, and gut microbiota dysbiosis associated
Summary
The obesity epidemic has spread globally in the past four decades. Nowadays, more than a third of the world population is obese or overweight [1,2]. Obesity is associated with a chronic inflammation that persists in the visceral adipose tissue (VAT) [9] In this regard, adipose tissue inflammation and oxidative stress lead to reduced production of adiponectin as well as increased secretion of resistin, leptin, and pro-inflammatory adipokines and cytokines, contributing to cardiovascular stiffness, an impaired vascular relaxation, and to cardiac diastolic dysfunction [5]. This review provides an update on the pathophysiology of obesity-associated CVD, including the role of PPARs, inflammatory and oxidative processes, gut microbiota dysbiosis, and offers concise information about epigenetic modifications in CVD. Likewise, this manuscript provides information on some experimental models used to study CVD.
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