Alteration in Inflammation-related miR-146a Expression in NF-KB Signaling Pathway in Diabetic Rat Hippocampus

Voluntary Exercise Protects Heart from Oxidative Stress in Diabetic Rats

Swim Training Improves HOMA-IR in Type 2 Diabetes Induced by High Fat Diet and Low Dose of Streptozotocin in Male Rats

Background: Sirtuin1 is a regulator of oxidative stress involved in the management of diabetes complications. Due to the beneficial effects of swimming training in diabetes, this study aimed to investigate the effects of swimming training on pancreatic Sirtuin1, oxidative stress and metabolic parameters in type 2 diabetic male rats. Materials and methods: Twenty-eight male Wistar rats (200–250 g) were randomly divided into four groups: control, diabetic, swim trained and swim trained diabetic rats (n = 7). Diabetes was induced by a high-fat diet and streptozotocin injection [35/kg intraperitoneally]. After 72 hours, animals with blood glucose levels ≥300 mg/dL were considered diabetic. Seven days after the induction of diabetes, animals in the exercise groups were subjected to swimming training (60 min/daily, 5 days/week) for 12 weeks. At the end of the intervention, the animals were anesthetized, and tissue/blood samples were prepared for measurements of metabolic parameters, albumin, the Sitruin1 gene and its protein expression levels, oxidative stress and histological study. Results: This study indicated that the diabetic rats had a significant decrease (p < 0.01, p < 0.05) in pancreatic Sitruin1 gene and its protein expression levels, antioxidant enzymes, serum albumin, and the quantitative insulin sensitivity check index, but a significant increase (p < 0.01) in malondialdehyde level. Swimming training resulted in a considerable improvement (p < 0.01, p < 0.05) in pancreatic Sitruin1 gene and its protein expression levels, antioxidant enzymes, serum levels of albumin and metabolic parameters. In addition, histological findings indicated the beta-cells conservation. Conclusions: This study suggested that pancreatic Sitruin1 may be a promising therapeutic target for diabetic complications.

Diabetes mellitus (DM) is one of the major risk factors for cardiovascular disease, leading to endothelial dysfunction and angiogenesis impairment . MiR-126 and miR-210 support angiogenic response in endothelial cells. The present study sought to explore the effect of garlic and voluntary exercise, alone or together, on miR-126 and miR-210 expressions and cardiac angiogenesis in rats with type 1 diabetes. Male Wistar rats were divided into five groups (n = 7): Control, Diabetes, Diabetes+Garlic, Diabetes+Exercise, and Diabetes+Garlic+Exercise. Diabetes was induced in the animals by streptozotocin (ip, 50 mg/kg). The rats were then fed raw fresh garlic homogenate (250 mg/kg) or were subjected to voluntary exercise, or to combined garlic and voluntary exercise for 6 weeks. MiR-126 and miR-210 expressions in the myocardium were determined by real time PCR, and the serum lipid profile was measured by enzymatic kits. Angiogenesis was evaluated by immunostaining for PECAM-1/ CD31 in the myocardium. Diabetes reduced both cardiac miR-126 expression and angiogenesis (p < 0.05). On the other hand, there was a miR-210 expression increase in the myocardium of diabetic animals (p < 0.001). However, those effects reversed either with garlic or voluntary exercise (p < 0.01). Moreover, treating diabetic rats with garlic and voluntary exercise combined had an additional effect on the expressions of miR-126 and miR-210 (p < 0.001). Furthermore, both voluntary exercise and garlic significantly improved serum lipid profiles (p < 0.001). The induction of diabetes decreased angiogenesis in the myocardium, whereas our treatment using long-term voluntary exercise and garlic improved myocardial angiogenesis. These changes were possibly owing to the enhancement of myocardial miR-126 and miR-210 expressions.

Introduction: Obesity resulted by imbalance between the intake of energy and energy consumption can lead to growth and metabolic disease development in people. Both in obese men and animal models, several studies indicate that obesity leads to male infertility.Objective: This review has discussed some mechanisms involved in obesity-induced male infertility.Method: Online documents were searched through Science Direct, Pubmed, Scopus, and Google Scholar websites dating from 1959 to recognize studies on obesity, kisspeptin, leptin, and infertility.Results: Obesity induced elevated inflammatory cytokines and oxidative stress can affect male reproductive functions, including spermatogenesis disorders, reduced male fertility power and hormones involved in the hypothalamus-pituitary-gonadal axis.Conclusion: There is significant evidence that obesity resulted in male infertility. Obesity has a negative effect on male reproductive function via several mechanisms such as inflammation and oxidative stress.