The present study aims at exploring the effects of sardine protein on insulin resistance, plasma lipid profile, as well as oxidative and inflammatory status in rats with fructose-induced metabolic syndrome. Rats were fed sardine protein (S) or casein (C) diets supplemented or not with high-fructose (HF) for 2 months. Rats fed the HF diets had greater body weight and adiposity and lower food intake as compared to control rats. Increased plasma glucose, insulin, HbA1C, triacylglycerols, free fatty acids and impaired glucose tolerance and insulin resistance was observed in HF-fed rats. Moreover, a decline in adipose tissues antioxidant status and a rise in lipid peroxidation and plasma TNF-α and fibrinogen were noted. Rats fed sardine protein diets exhibited lower food intake and fat mass than those fed casein diets. Sardine protein diets diminished plasma insulin and insulin resistance. Plasma triacylglycerol and free fatty acids were also lower, while those of α-tocopherol, taurine and calcium were enhanced as compared to casein diets. Moreover, S-HF diet significantly decreased plasma glucose and HbA1C. Sardine protein consumption lowered hydroperoxide levels in perirenal and brown adipose tissues. The S-HF diet, as compared to C-HF diet decreased epididymal hydroperoxides. Feeding sardine protein diets decreased brown adipose tissue carbonyls and increased glutathione peroxidase activity. Perirenal and epididymal superoxide dismutase and catalase activities and brown catalase activity were significantly greater in S-HF group than in C-HF group. Sardine protein diets also prevented hyperleptinemia and reduced inflammatory status in comparison with rats fed casein diets. Taken together, these results support the beneficial effect of sardine protein in fructose-induced metabolic syndrome on such variables as hyperglycemia, insulin resistance, hyperlipidemia and oxidative and inflammatory status, suggesting the possible use of sardine protein as a protective strategy against insulin resistance and related situations.
Abstract. The present study explored the potential of fish proteins to counteract high glucose levels and oxidative stress induced by fructose in the brain. A total of 24 male Wistar rats consumed sardine protein or casein with or without high fructose (64%). After 2 months, brain tissue was used for analyses. The fructose rats exhibited an increase in body mass index (BMI), body weight, absolute and relative brain weights and brain glucose; however, there was a decrease in food and water intake. Fructose disrupts membrane homeostasis, as evidenced by an increase in the brain hydroperoxides and a decrease in catalase (CAT) and glutathione peroxidase (GSH-Px) compared to the control. The exposure to the sardine protein reduced BMI, food intake, glucose and hydroperoxides, and increased CAT and GSH-Px in the brain. In conclusion, the metabolic dysfunctions associated with the fructose treatment were ameliorated by the presence of sardine protein in the diet by decreasing BMI, brain glucose and lipid peroxidation, and increasing CAT and GSH-Px activities.
Abstract. The current study investigated whether sardine protein mitigates the adverse effects of fructose on plasma glucagon-like peptide-1 (GLP-1) and oxidative stress in rats. Rats were fed casein (C) or sardine protein (S) with or without high-fructose (HF) for 2 months. Plasma glucose, insulin, GLP-1, lipid and protein oxidation and antioxidant enzymes were assayed. HF rats developed obesity, hyperglycemia, hyperinsulinemia, insulin resistance and oxidative stress despite reduced energy and food intakes. High plasma creatinine and uric acid levels, in addition to albuminuria were observed in the HF groups. The S-HF diet reduced plasma glucose, insulin, creatinine, uric acid and homeostasis model assessment-insulin resistance index levels, however increased GLP-1 levels compared with the C-HF diet. Hydroperoxides were reduced in the liver, kidney, heart and muscle of S-HF fed rats compared with C-HF fed rats. A reduction in liver, kidney and heart carbonyls was observed in S-HF fed rats compared with C-HF fed rats. Reduced levels of nitric oxide (NO) were detected in the liver, kidney and heart of the S-HF fed rats compared with C-HF fed rats. The S diet compared with the C diet reduced levels of liver hydroperoxides, heart carbonyls and kidney NO. The S-HF diet compared with the C-HF diet increased the levels of liver and kidney superoxide dismutase, liver and muscle catalase, liver, heart and muscle glutathione peroxidase and liver ascorbic acid. The S diet prevented and reversed insulin resistance and oxidative stress, and may have benefits in patients with metabolic syndrome.
Metabolic syndrome is associated with several disorders, including hypertension, diabetes, hyperlipidemia as well as cardiovascular diseases and stroke. The purpose of the present study was to investigate the preventive effect of Rubus ulmifolius Schott extract (E) on hyperglycemia, hyperlipidemia and liver oxidative stress in rats fed a high-sucrose diet.Male Wistar rats (n = 21) weighing 115 ± 3 g were used in this experiment. For induction of MS, fourteen rats were given free access to 60% sucrose in drinking water and seven rats received water for 3 weeks. After this induction phase, rats were assigned to three equal-weight groups as follows: 1) C: rats were kept on standard pellet diet. 2) HSD: rats were kept on high-sucrose diet containing 60% sucrose for 3 weeks. 3) HSD + E: rats were kept on HSD and orally administered 300 mg/kg of extract by stomach tube once daily for a period of 3 weeks.Rats exposed to a sucrose-rich diet exhibited similar body weight despite lower food intake when comparing to control rats. Increased plasma glucose, HbA1C, triglycerides, total cholesterol (TC), VLDL-C, LDL-C, TC-HDL-C/HDL-C, total protein, albumin, fibrinogen, urea, uric acid, creatinine, ALT, AST, decreased HDL-C and impaired tolerance to glucose was reported in HS-fed rats. We also observed high TBARS and low SOD, CAT and GSH-Px activities in liver. Supplementation of HS diet with Rubus ulmifolius Schott extract at a 300 mg/kg dose improved glucose tolerance, hyperglycemia, HbA1c, dyslipidemia, liver and renal abnormalities and liver oxidative stress when compared to HSD rats.Taken as a whole, these results support the favorable effect of Rubus ulmifolius Schott extract in sucrose-induced metabolic syndrome on such variables as hyperglycemia, glucose tolerance, lipid metabolism, and liver oxidative damage, suggesting that Rubus ulmifolius Schott could be beneficial to counteract deleterious dietary sucrose in an animal metabolic syndrome model.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.