Protective effects of either C‐peptide or l‐arginine on pancreatic β‐cell function, proliferation, and oxidative stress in streptozotocin‐induced diabetic rats

Abstract

Diabetes and cardiometabolic risk factors including hypertension and dyslipidemia are the major threats to human health in the 21st century. Apoptosis in pancreatic tissue is one of the major causes of diabetes type 1 progression. The aim of this study was to investigate the effects of C‐peptide or l‐arginine on some cardiometabolic risk factors, pancreatic morphology, function and apoptosis, and the mechanisms of their actions. Forty adult male albino rats were divided into four equal groups: 1—control nondiabetic, 2—diabetic (no treatment), 3—diabetic + C‐peptide, and 4—diabetic + l‐arginine. Diabetes was induced by a single intraperitoneal injection of high dose streptozotocin. At the end of the experiment, sera glucose, insulin levels, total antioxidant capacity (TAC), malondialdehyde (MDA), nitric oxide (NO), and pancreatic MDA, TAC, and B‐cell lymphoma 2 were measured. The morphology and proliferating activity of the pancreas were examined by hematoxylin and eosin histological stain, proliferative cell nuclear antigen (PCNA), and insulin antibodies. Our results showed that induction of diabetes caused hyperglycemia, dyslipidemia, and oxidative stress. However, administration of C‐peptide or l‐arginine significantly improved the pancreatic histopathology with a significant increase in the area % of insulin immunoreactivity, the number of PCNA immunopositive cells, the number of islets, and the diameter of islets compared with the diabetic group. C‐peptide treatment of the diabetic rats completely corrected these errors, while l‐arginine partially antagonized the above diabetic complications. So the administration of C‐peptide as an adjuvant therapy in type 1 diabetes can significantly decrease apoptosis of pancreas and subsequent progression of diabetes complication.

Evaluation the effects of insulin on oxidant/antioxidant status in type 1 diabetic patients

“…Therefore, the rise in insulin resistance in insulin-treated patients may be due to poor glycaemic control, which in turn reduces insulin action by lowering the level of nitric oxide (Mohammad et al 2021). Previous studies have revealed that nitric oxide contributes to the effect of insulin via intracellular mechanisms (Ding et al 2000;Kocic et al 2007;Ragy and Ahmed 2019). The correlation between FSG and HO-MA-IR observed in this study further confirms the role of hyperglycaemia in increasing insulin resistance.…”

Bee venom attenuates degenerative effects of diabetes associated with hyperlipidemia in rats.

“…Our results stated that levels of pancreatic, hepatic, and renal total antioxidant capacity (TAC) were decreased significantly in the positive control group compared to the negative control group. These results are in harmony with previous studies [92][93][94] which described that total antioxidant levels in the pancreas, liver, and kidney were reduced in diabetic rats because hyperglycemia is associated with an imbalance between reactive oxygen species production and antioxidant defense mechanism. While the levels of pancreatic, hepatic, and renal total antioxidant capacity (TAC) were significantly increased (0.5 and 1.23 mg/kg) and in Metformin and Atorvastatin treated group compared to positive control.…”

Dietary N-carbamylglutamate and L-arginine supplementation improves redox status and suppresses apoptosis in the colon of intrauterine growth-retarded suckling lambs

“…Arginine is a powerful stimulator of insulin secretion ( Ragy and Ahmed, 2019 ). Hence, nutrient use efficiency can be improved in part by enhancing concentrations of anabolic hormones in the intestine and the ensuing increase in tissue protein synthesis ( Yao et al., 2011 ).…”