The role of oxidative stress on the pathophysiology of metabolic syndrome

Abstract

The role of oxidaTive sTress on The paThophysiology of meTabolic syndrome rev assoc Med Bras 2017; 63(1):85-91 85 REVIEW ARTICLEThe role of oxidative stress on the pathophysiology of metabolic syndrome Metabolic syndrome (MetS) has a high prevalence around the world. Considering the components used to classify MetS, it is clear that it is closely related to obesity. These two conditions begin with an increase in abdominal adipose tissue, which is metabolically more active, containing a greater amount of resident macrophages compared to other fat deposits. Abdominal adiposity promotes inflammation and oxidative stress, which are precursors of various complications involving MetS components, namely insulin resistance, hypertension and hyperlipidemia. One way to block the effects of oxidative stress would be through the antioxidant defense system, which offsets the excess free radicals. It is known that individuals with metabolic syndrome and obesity have high consumption of fats and sugars originated from processed foods containing high levels of sodium as well as low intake of fruits and vegetables, thus maintaining a state of oxidative stress, that can speed up the onset of MetS. Healthy eating habits could prevent or delay MetS by adding antioxidant-rich foods into the diet.

Association of lipid peroxidation and antioxidant status with metabolic syndrome in Iranian healthy elderly women

“…Evidence suggests that OxS is increased in the case of metabolic syndrome (MetS) due to fat accumulation (4). Dyslipidemia and insulin resistance (IR) associated with MetS increases the production of reactive oxygen species and consequently raises the oxidation of lipid products, DNA and proteins, which in turn lead to endothelium dysfunction, cancer and other chronic diseases related to aging (5,6).…”

The effect of cumin supplementation on metabolic profiles in patients with metabolic syndrome: A randomized, triple blind, placebo‐controlled clinical trial

“…ROS, which are induced by MetS, have a direct role in the initiation of oxidative stress, oxidation of lipids, formation of advanced glycation end products, and inflammation (Hopps et al, ). Protein kinase C, mitogen‐activated protein kinase, nuclear factor kappa‐light‐chain‐enhancer of activated B cells, transforming growth factor‐ β 1 and monocyte chemoattractant protein‐1 are involved in the pathogenicity of ROS (Francisqueti et al, ; Monteiro & Azevedo, ; Otani, ). Several in vitro studies have proposed beneficial effects of CuEO as an antioxidant and lipid peroxidation inhibitor (Chen et al, ; Hopps et al, ; Moghadam, ).…”

“…Metabolic syndrome (MetS), recognized as syndrome X or insulin resistance syndrome, is characterized by dyslipidemia, hypertension, hyperglycemia, and central obesity (Francisqueti et al, ). It causes fivefold increase in the risk of Type 2 diabetes mellitus (Alberti et al, ) and is associated with an increased mortality from cardiovascular disease (Isomaa et al, ).…”

“…The components of MetS are closely associated with an increased oxidative stress (Hopps, Noto, Caimi, & Averna, ). Oxidants commonly known as free radicals including reactive oxygen and nitrogen species cause oxidation of lipids (Francisqueti et al, ), which can generate malondialdehyde (MDA; Aldini, Dalle‐Donne, Facino, Milzani, & Carini, ). Endogenous antioxidant enzymes and low‐molecular‐weight scavengers such as glutathione peroxidase (GSH‐Px), superoxide dismutase (SOD), uric acid, coenzyme Q, and lipoic acid control the oxidative stress (Poljsak, Šuput, & Milisav, ).…”

Liver mitochondrial membrane permeability modulation in insulin-resistant, uninephrectomised male rats by Clerodendrum volubile P. Beauv and Manihot esculenta Crantz

“…The situation arising from sinusoidal stasis leads to cell death among other clinical manifestations [11] [12]. Mitochondrial dysfunction and oxidative stress associated with metabolic syndrome have been proposed as major pathophysiological disturbances that contribute to these pathologies [13,14].…”