High fat diet (HFD) and low dose of streptozotocin (STZ)-treated rats provide an animal model for type 2 Diabetes Mellitus (T2DM). Oxidative stress plays a role in the development of diabetic complications. Carnosine (CAR) has antioxidant and antiglycating properties. We investigated effects of CAR on renal function, oxidation and glycation products in HFD+STZ-rats. Rats were fed with HFD (60% of total calories from fat) for 4 weeks and then a single dose STZ (40 mg/kg; i.p.) was applied. Rats with blood glucose levels above 200 mg/dL were fed with HFD until the end of the 12th week. CAR (250 mg/kg body weight; i.p.; 5 times a week) was administered to rats for the last 4 weeks. Glycated hemoglobin (HbA1c), glucose, lipids, and andrenal function tests in serum as well as reactive oxygen species, malondialdehyde, protein carbonyl, advanced oxidation protein products, advanced glycation end products (AGEs), antioxidant power, and antioxidant enzyme activities and their mRNA expressions in kidneys were determined. CAR treatment did not alter glucose and HbA1c, but it decreased serum lipids, creatinine, and urea levels in HFD+STZ rats. Oxidation products of lipids and proteins and AGEs levels decreased, but antioxidant enzyme activities and their mRNA expressions remained unchanged due to CAR treatment. Our results indicate that CAR treatment alleviated renal function and decreased accumulation of oxidation and glycation products in kidneys in HFD+STZ-rats.
23 May 2024 in Clinical Psychopharmacology and Neuroscience
The effect of N-acetylcysteine (NAC) (1 g/kg body weight/day) on serum homocysteine (Hcy) levels, insulin resistance (IR), and hepatic and renal prooxidant-antioxidant balance was evaluated in rats treated with homocysteine thiolactone (HcyT) (500 mg/kg body weight/day for 6 weeks). Reactive oxygen species (ROS), malondialdehyde (MDA), glutathione, ferric reducing antioxidant power, and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were determined in the liver and kidney. HcyT elevated serum Hcy levels and caused IR, but liver and kidney function tests remained unchanged. HcyT increased ROS and MDA without any change in hepatic antioxidants, but it elevated renal SOD and GSH-Px activities. NAC decreased serum Hcy, hepatic and renal ROS and MDA levels, and renal SOD and GSH-Px activities in rats with high Hcy levels. However, it did not ameliorate IR. Our results indicate that NAC supplementation may be effective in decreasing Hcy levels and Hcy-induced hepatic and renal oxidative stress.
Objective: The present study was aimed to investigate the effects of betaine (BET) on streptozotocin (STZ)-induced diabetes mellitus (DM) in rats. Additionally, the efficiency of BET was compared with metformin (MET), a standard oral antidiabetic drug. Methods: STZ (55 mg/kg body weight; i.p.) was injected to male Wistar rats. Rats with DM were treated with BET (1 g/kg body weight/day;) or MET (500 mg/kg body weight/day;) for 4 weeks. Blood glycated hemoglobin (HbA 1c ), serum glucose, lipids, hepatic and renal function tests and urinary protein levels were examined. Reactive oxygen species (ROS) formation, malondialdehyde (MDA), glutathione (GSH) levels, and ferric reducing antioxidant power (FRAP) were also determined in liver and kidney. Results: Glucose, HbA 1c , and serum lipids increased and liver and kidney function tests were impaired in diabetic rats. Hepatic and renal ROS formation and MDA levels were elevated, hepatic, but not renal GSH and FRAP levels were decreased. BET decreased blood HbA 1c , serum glucose and lipid levels and urine protein levels. BET diminished hepatic and renal prooxidant status. Conclusion: Our results indicate that BET may be effective in decreasing STZ-induced high levels of blood HbA 1c , and serum glucose and lipid levels and prooxidant status in liver and kidney tissues.