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

Hala Mourad Demerdash*

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

ROS stimulates the production of inflammatory cytokines, which further exacerbate ROS release, thus establishing a vicious circle, promoting increased adipocyte proliferation, differentiation.3
Inability of body to eradicate excessive ROS as result of diminution in antioxidant defense and subsequent imbalance in antioxidant defense; may be a major factor in the pathogenesis
of obesity co-morbidities.

Insulin inactivity caused by down regulation of insulin receptor IRS expression and inhibition of insulin action affects pancreatic acinar cells, resulting in loss of insulinotropic action on these cells, together with decreased secretion of pancreatic enzymes as pancreatic amylase. Therefore, insulin resistance is associated with low serum amylase levels, since endogenous insulin potentiates zymogen release. Similarly, low-levels of pancreatic lipase which hydrolyzes digested fat.

First, various inflammatory cytokines from adipose tissue impair insulin signaling, coupled with increased release of transcription factors, including adipocyte differentiation factor 1/sterol regulatory element-binding protein-1c (SREBP1-c), that regulates the expression of several genes responsible for adipocyte differentiation, lipogenesis, lipolysis and fatty acid oxidation. Inflammatory cytokines as TNF-α also stimulates ceramide accumulation by activating sphingomyelinase, an enzyme that catalyzes the hydrolysis of sphingomyelin to ceramide.

Obes Res Open J. 2017; 4(2): 32-43.doi: 10.17140/OROJ-4-131