A Longitudinal Study of the Antioxidant Barrier and Oxidative Stress in Morbidly Obese Patients after Bariatric Surgery. Does the Metabolic Syndrome Affect the Redox Homeostasis of Obese People?

Abstract

This is the first study to evaluate both the antioxidant barrier, glutathione metabolism, and oxidative damage to proteins and lipids in morbidly obese patients undergoing bariatric treatment. The study included 65 patients with class 3 obesity divided into two subgroups: morbidly obese patients without metabolic syndrome (OB) and obese patients with metabolic syndrome (OB + MS). Blood samples were collected before surgery as well as one, three, six, and twelve months after the bariatric treatment. Superoxide dismutase and reduced glutathione (GSH) were significantly decreased, whereas glutathione reductase and uric acid were enhanced in morbidly obese patients before bariatric surgery as compared to lean control. Moreover, in the OB group, we observed the increase of superoxide dismutase (SOD) and the decrease of uric acid (UA) after the bariatric treatment; however, these changes were not observed in the OB + MS group. The oxidative damage to proteins (advanced glycation end products, AGE; advanced oxidation protein products, AOPP) and lipids (8-isoprostanes, 8-isop; 4-hydroxynoneal) was higher in OB as well as OB + MS patients. We noticed that AGE and AOPP levels diminished after the bariatric treatment, whereas redox status (ratio of GSH to oxidized glutathione) was still reduced in the OB + MS group. Summarizing, morbid obesity is associated with disturbances in the antioxidant barrier and enhanced oxidative damage to proteins and lipids. Although bariatric surgery improves redox homeostasis in obese patients, those with metabolic syndrome show a continuous decrease in the antioxidant status. In patients undergoing bariatric treatment, antioxidant supplementation may be considered.

Impact of Weight Loss on the Total Antioxidant/Oxidant Potential in Patients with Morbid Obesity—A Longitudinal Study

“…Indeed, there have been only a few studies of the impact of surgical treatment on pro-oxidant/antioxidant homeostasis. In our previous research, we found disturbances in enzymatic and non-enzymatic antioxidant status, which partially normalized after bariatric surgery [19]. Serum superoxide dismutase (SOD) and plasma-reduced glutathione (GSH) were significantly diminished in both obese groups before bariatric surgery, while uric acid (UA) and glutathione disulfide (GSSG) were statistically higher.…”

“…The World Health Organization (WHO) estimates that at least 3 million people worldwide die each year from obesity-related complications [2]. Numerous studies suggest that metabolic diseases accompanying obesity can be caused not only by a higher accumulation of bioactive lipids [28,29], but also by disturbances in pro-oxidant/antioxidant balance [19,30]. Indeed, both increase and decrease of the antioxidant barrier have been observed in morbidly obese patients [28,31,32].…”

“…However, higher oxidative damage to proteins, lipids, and DNA was observed in patients with morbid obesity. Increased levels of oxidative modification products were found not only in plasma but also in skeletal muscles, adipose tissue, liver, and salivary glands [19,[37][38][39]. How then to explain the increase in total antioxidant potential in obese patients?…”

“…It can be assumed that antioxidant systems are activated in the early stages of the disease. With the long-term development of obesity, the source of antioxidants gradually depletes, leading to a reduced activity of the antioxidant barrier [19,43]. However, it can be assumed that hyperuricemia is mainly responsible for disturbances in plasma redox status of obese patients.…”

“…In our previous study, we demonstrated abnormalities of the enzymatic and non-enzymatic antioxidant barrier, which partially persist after bariatric surgery [19]. Although some of the redox parameters were normalized after the procedure and some were not, the total antioxidant/oxidant potential change in patients with morbid obesity is still unknown.…”