Effects of lycopene on plasma glucose, insulin levels, oxidative stress, and body weights of streptozotocin-induced diabetic rats

To determine possible therapeutic effects of oral lycopene supplementation on plasma insulin levels, lipid peroxidation, blood glucose levels, and the antioxidant defense system of streptozotocin-induced diabetic rats. Materials and methods: Classical biochemical methods were used to determine plasma malondialdehyde (MDA), nitric oxide (NO), glutathione peroxidase (GSH-Px), catalase (CAT), superoxide dismutase (SOD), and glutathione (GSH) levels. Enzyme-linked immunosorbent assay was used to determine plasma insulin levels and reverse transcriptase-polymerase chain reaction was used to determine the levels of brain antioxidant enzymes (SOD, CAT, and GSH-Px). Results: It was found that the diabetes-related increase in blood glucose levels was reduced by supplementation of lycopene over an 8-week period. Plasma NO levels and brain tissue GSH levels were meaningfully reduced in the treatment group compared to the diabetic group. In the hemolysate samples, it was determined that the treatment group's SOD, CAT, and GSH-Px activities significantly increased compared to the diabetic group. In the brain tissue homogenates, CAT and SOD activity did not show a significant change, whereas GSH-Px activity was increased in the treatment group compared to the diabetic group. SOD, CAT, and GSH-Px mRNA transcription levels were suppressed in the diabetic group compared to the control, and this suppression was stopped and increases were significantly induced by the supplementation of lycopene. Conclusion: In this study, the oxidative damage and low insulin levels associated with diabetes were ameliorated with the administration of lycopene. The results of this study indicate that lycopene is an effective nutritional component to alleviate and/or prevent the complications of diabetes, and these findings can be used as a basis for future studies.

Effects of lycopene on plasma glucose, insulin levels, oxidative stress, and body weights of streptozotocin-induced diabetic rats

To determine possible therapeutic effects of oral lycopene supplementation on plasma insulin levels, lipid peroxidation, blood glucose levels, and the antioxidant defense system of streptozotocin-induced diabetic rats. Materials and methods: Classical biochemical methods were used to determine plasma malondialdehyde (MDA), nitric oxide (NO), glutathione peroxidase (GSH-Px), catalase (CAT), superoxide dismutase (SOD), and glutathione (GSH) levels. Enzyme-linked immunosorbent assay was used to determine plasma insulin levels and reverse transcriptase-polymerase chain reaction was used to determine the levels of brain antioxidant enzymes (SOD, CAT, and GSH-Px). Results: It was found that the diabetes-related increase in blood glucose levels was reduced by supplementation of lycopene over an 8-week period. Plasma NO levels and brain tissue GSH levels were meaningfully reduced in the treatment group compared to the diabetic group. In the hemolysate samples, it was determined that the treatment group's SOD, CAT, and GSH-Px activities significantly increased compared to the diabetic group. In the brain tissue homogenates, CAT and SOD activity did not show a significant change, whereas GSH-Px activity was increased in the treatment group compared to the diabetic group. SOD, CAT, and GSH-Px mRNA transcription levels were suppressed in the diabetic group compared to the control, and this suppression was stopped and increases were significantly induced by the supplementation of lycopene. Conclusion: In this study, the oxidative damage and low insulin levels associated with diabetes were ameliorated with the administration of lycopene. The results of this study indicate that lycopene is an effective nutritional component to alleviate and/or prevent the complications of diabetes, and these findings can be used as a basis for future studies.
Turkish Journal of Medical Sciences-Cover
  • ISSN: 1300-0144
  • Yayın Aralığı: Yılda 6 Sayı
  • Yayıncı: TÜBİTAK
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