Key result
A high-fat, high-carbohydrate diet in male rats induced metabolic syndrome and shifted adipocyte redox balance toward oxidative stress, decreasing the GSH/GSSG ratio and antioxidant enzyme activity.
Why the study?
The study aimed to evaluate the functional state of the glutathione-dependent antioxidant system components in the adipose tissue of rats with experimental metabolic syndrome.
Does a high-fat, high-carbohydrate diet alter the functional state of the glutathione-dependent antioxidant system in the adipose tissue of rats?
Does a high-fat, high-carbohydrate diet alter the functional state of the glutathione-dependent antioxidant system in the adipose tissue of rats?
Experimental metabolic syndrome induced by a high-fat, high-carbohydrate diet in rats causes a shift in adipocyte redox balance toward oxidative stress, characterized by decreased glutathione-dependent antioxidant defenses.
Rat MetS model findings on adipose glutathione system need human validation; leaves open antioxidant targeting in clinical MetS.
Aim : To study the functional state of the components of the glutathione-dependent antioxidant system in the adipose tissue of rats with experimental metabolic syndrome (MetS). Material and Methods . The MetS model was carried out on male Wistar rats using a high-fat, high-carbohydrate diet (HFHCD). Body and adipose tissue weight were measured. Blood serum levels of glucose, insulin, leptin, triacylglycerides and cholesterol were assessed. In epididymal adipose tissue the level of reactive oxygen species (ROS) was determined by fluorescent method. The concentration of reduced (GSH) and oxidized (GSSG) glutathione, activity of glutathione reductase, glutathione peroxidase, and glutathione-S-transferase enzymes were assessed spectrophotometrically in epididymal adipose tissue. Results . It was found that HFHCD led to an increase in body weight, obesity, hyperglycemia, insulin resistance, dyslipidemia, and leptinemia in the experimental group rats. An increase in adipose tissue mass had a positive correlation with an increase in the concentration of glucose, serum leptin, and ROS levels in the epididymal adipose tissue of rats with MetS. It was found that the level of total glutathione in the adipose tissue of the experimental group rats decreased mainly due to a decrease in the level of GSH. The rats receiving HFHCD also showed a decrease in the activity of glutathione peroxidase and glutathione-S-transferase, but the activity of glutathione reductase increased. Conclusion . Obesity, as a key component of MetS, is a trigger of insulin resistance, chronic low-grade inflammation and oxidative stress. The study showed that the development of MetS and obesity in the experimental animal group is accompanied by a shift of adipocyte redox balance toward oxidative stress, which is expressed in a decrease of GSH/GSSG ratio and glutathione-dependent antiperoxide protection enzymes activity.
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Birulina et al. (2023) studied Metabolic syndrome. High-fat, high-carbohydrate diet (HFHCD) vs. Control diet was evaluated on Functional state of the components of the glutathione-dependent antioxidant system in adipose tissue. A high-fat, high-carbohydrate diet in male rats induced metabolic syndrome and shifted adipocyte redox balance toward oxidative stress, decreasing the GSH/GSSG ratio and antioxidant enzyme activity.
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