Role of Oxidative Stress and Associated Alteration in Enzyme Activities in Obesity Comorbidities

Abstract

Citation Review ABSTRACTObesity is defined as having a body mass index (BMI) of 30 kg/m 2 or above, with progressively increasing prevalence all over the world in recent years. Obesity is characterized by deposition of abnormally increased body fat, resulting from increased energy intake relative to energy expenditure. The condition is associated with several comorbidities that upsurge risk of morbidity. The purpose of this review is to describe the role of oxidative stress in release of pro-inflammatory mediators that influence fat and glucose metabolism and is associated with altered enzyme activity, which results in insulin resistance and other associated comorbidities. The main pathology is through intensified generation of reactive oxygen species (ROS) and diminution of antioxidant defense, creating a chronic inflammatory situation that is critically important in development of comorbidities. New strategies to combat resultant comorbidities concentrate on weight reduction either solely or coupled with moderately regular exercise. This policy may be sufficient to improve insulin sensitivity, regulate fatty acid metabolism together with refining antioxidant defense of the body. Other approaches encourage modulation of dietary pattern through dietary supplements as vitamins, with or without pharmaceutical antioxidants, which may provide a potential therapeutics approach in obesity comorbidities

Oxidative Imbalance and Kidney Damage in Cafeteria Diet-Induced Rat Model of Metabolic Syndrome: Effect of Bergamot Polyphenolic Fraction

“…Concerning enzymatic antioxidants, regulation mechanisms are more complex: in the case of low/medium oxidative stimulation, enzymatic antioxidant activity can increase, but, if oxidative stress is persisting, or its level is very high, the damage caused to proteins becomes profound and a decreased expression/activity may occur via direct oxidative damage of the molecules and/or oxidative-altered gene expression. Alterations in the enzymatic antioxidant defense mechanisms are reported in obesity models including human, but the described scenario is very intricate [60]. In obese mice, expression levels and activities of antioxidant enzymes decreased particularly at adipose tissue level [61] while the levels of antioxidant enzymes in hamsters were not greatly modified by CAF diet-induced obesity [62].…”

Oxidative Imbalance and Kidney Damage: New Study Perspectives from Animal Models to Hospitalized Patients

“…It is well known that increased oxidative stress in metabolic disorders (diabetes, obesity, and dyslipidemia) implies nonenzymatic antioxidant depletion [58], and this is the first detectable event of a redox disturbance (as has been highlighted by our research group in humans as well) [81,82]. In obesity models, the enzymatic antioxidant defenses turn out to be altered, but the scenario is very complex and dissimilar in different organs and tissues [83][84][85]. In renal tissues in our obesity model, we found no changes in the expression of SOD1, the most important preventive antioxidant, while there was a considerable and significant decrease in the GSTP1 monomer (the form with antioxidant and proliferative activity).…”