Cardiovascular consequences of metabolic syndrome

Abstract

The metabolic syndrome (MetS) is defined as the concurrence of obesity-associated cardiovascular risk factors including abdominal obesity, impaired glucose tolerance, hypertriglyceridemia, decreased HDL cholesterol, and/or hypertension. Earlier conceptualizations of the MetS focused on insulin resistance as a core feature, and it is clearly coincident with the above list of features. Each component of the MetS is an independent risk factor for cardiovascular disease and the combination of these risk factors elevates rates and severity of cardiovascular disease, related to a spectrum of cardiovascular conditions including microvascular dysfunction, coronary atherosclerosis and calcification, cardiac dysfunction, myocardial infarction, and heart failure. While advances in understanding the etiology and consequences of this complex disorder have been made, the underlying pathophysiologic mechanisms remain incompletely understood, and it is unclear how these concurrent risk factors conspire to produce the variety of obesity-associated adverse cardiovascular diseases. In this review we highlight current knowledge regarding the pathophysiologic consequences of obesity and the MetS on cardiovascular function and disease, including considerations of potential physiologic and molecular mechanisms that may contribute to these adverse outcomes.

The Vascular Consequences of Metabolic Syndrome: Rodent Models, Endothelial Dysfunction, and Current Therapies

“…Another characteristic of metabolic syndrome is chronic low-grade inflammation (De Ferranti and Mozaffarian, 2008;Sharma, 2011). These factors all contribute to the elevated risk of cardiovascular disease, acute cardiovascular events (including stroke and myocardial infarction), type 2 diabetes mellitus (T2DM), or further complications such as renal disease (O'Neill and O'Driscoll, 2015;Tune et al, 2017). Vascular dysfunction is a key contributor to the pathogenesis of all of these disorders (Rajendran et al, 2013).…”

Is insulin pro-atherogenic at the cellular level?

“…Since hyperinsulinemia is associated with increased cardiovascular risk, hyperinsulinemia and hepatic portal hypoinsulinemia due to injection of insulin preparations widely used in the treatment of type 1 diabetic patients could be responsible, at least in part, for cardiovascular consequences of the disease. The results of epidemiological studies and experimental studies in animal models supported systemic hyperinsulinemia as a major plausible factor in the development of atherosclerosis in diabetic patients [6][7][8][9][10] . Insulin resistance is strongly associated with hyperinsulinemia, and is considered as the major pathologic mechanism for susceptibility to premature atherosclerosis and cardiovascular disease [11,12] .…”

Mechanisms of Action of Kefir in Chronic Cardiovascular and Metabolic Diseases

“…There is a growing body of evidence [28][29][30] that the mechanisms underlying the effects of probiotics on the host gut include (a) production of antimicrobial substances (e.g., bacteriocins, microcins, defensins, free fatty acids and hydrogen peroxide), (b) competition for adhesion to the epithelium and for nutrients, (c) immunomodulatory actions and (d) inhibition of bacterial toxin production. All of these mechanisms are currently characterized and explored as important tools to alleviate the progression of gut microbiota disturbances and dysfunction of organs in the body.…”