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Inorganic nitrate supplementation is a possible therapeutic agent in diabetes. The aim of this study was to evaluate the effect of nitrate on the reproductive system in streptozotocin-induced diabetic male rats. Fifty male Wistar rats were allocated randomly to five groups: control (C), control plus nitrate (CN), diabetic (D), diabetic plus insulin (DI) and diabetic plus nitrate (DN). Sodium nitrate was administered for 2 months in the drinking water (100 mg l ) of the CN and DN groups. Insulin was injected at 2-4 U daily in the DI group. Serum glucose level and body weight were measured at the beginning of the study and at regular intervals. At the end of the study, serum levels of glucose, insulin, nitrogen oxides (NOx), luteinizing hormone (LH), follicle-stimulating hormone (FSH) and testosterone were assessed as well as sperm parameters, testis morphometry and histology, and testicular miR-34b and p53 mRNA expression. Nitrate treatment in diabetic rats significantly improved sperm parameters, epididymal weight, spermatogenesis and testicular histology as well as decreasing serum glucose and testicular p53 gene and miR-34b expression, although it had no effect on serum LH and FSH levels. In diabetic rats, serum insulin and NOx, body weight, testicular and epididymal weight, sperm count and motility, testis morphology, spermatogenesis indices, Johnsen's score, and testosterone were significantly lower than in controls. Nitrate administration increased serum insulin, NOx and testosterone levels in the DN group. Consuming water supplemented with sodium nitrate could improve diabetes-induced testicular functional and structural disorders; these favourable effects may be related to increased serum insulin and decreased serum glucose, as well as modulation of apoptosis in testis.

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Objective. Th e aim of this study was to assess whether microRNA-146a and its adapter proteins TNF receptor associated factor6 (TRAF6) and interleukin-1 receptor-associated kinase-1 (IRAK1) may be changed in the kidney of streptozotocin-induced diabetic rats, following regular moderate exercise.Methods. Forty adult male Wistar rats were allocated randomly into four groups (n=10), including sedentary control (SC), sedentary diabetic (SD), healthy sixty-day exercise (H60E), and diabetic sixty-day exercise (D60E) groups. Diabetes was induced by an intraperitoneal injection of 60 mg/kg streptozotocin. Aft er 48 h, blood glucose levels >250 mg/dl was included to diabetic rats. Aft er 2 days of diabetes induction, the exercise protocol began. Animals were exposed to 5 days of consecutive treadmill exercise for 60 min/day with the 22 m/min speed for 60 days. Th e kidneys of the rats were removed and microRNA was extracted from them using the miRCURYTM RNA isolation kit.Results. In diabetic rats, statistical analysis revealed a signifi cant decrease in miR-146a expression, non-signifi cant decrease in IRAK1 mRNA expression, and non-signifi cant increase in TRAF6 and NF-kB mRNA expression compared to the SC group. Exercise led to a non-signifi cant increase in the expression of miR-146a and NF-kB mRNA in the kidneys of the diabetic group as compared to the SD group, signifi cant increase in TRAF6 and IRAK1 mRNA expression compared to the H60E group, and signifi cant increase in TRAF6 mRNA expression compared to the SD group.Conclusion. Th e present data indicate that exercise might be able to help in the prevention in the diabetic nephropathy development.

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Purpose The purpose of the study was to evaluate the possible protective effects of low dose sodium nitrate preconditioning on the peripheral neuropathy in streptozotocin (STZ)-induced diabetic model. Methods Male Wistar rats were randomly divided into five groups: control (no intervention), control treated sodium nitrate (100 mg/L in drinking water), diabetic (no intervention), diabetic treated NPH insulin (2-4 U), and diabetic treated sodium nitrate (100 mg/L in drinking water). Diabetes was induced by intraperitoneal injection of STZ (60 mg/kg). All interventions were done for 60 days immediately following diabetes confirmation. Thermal and mechanical algesia thresholds were measured by means of hot-plate test, von Frey test, and tail-withdrawal test before the diabetic induction and after diabetes confirmation. At the end of the experiment, serum NOx level and serum insulin level were assessed. Blood glucose concentration and body weight have recorded at the base and duration of the experiment. Results Both hypoalgesia, hyperalgesia along with allodynia developed in diabetic rats. Significant alterations including, decrease in tail withdrawal latency (30th day), decreased mechanical threshold (60th day), and an increase in hot plate latency (61st day) were displayed in diabetic rats compared to control rats. Nitrate and insulin preconditioning produced protective effects against diabetesinduced peripheral neuropathy. Data analysis also showed a significant increase in glucose level as well as a considerable reduction in serum insulin and body weight of diabetic rats, which restored by both insulin and nitrate preconditioning. Conclusion Sodium nitrate preconditioning produces a protective effect in diabetic neuropathy, which may be mediated by its antihyperglycemic effects and increased serum insulin level. KeywordsNitrate preconditioning . Diabetes . Peripheral nerve . Thermal algesia . Mechanical algesia Highlights • Diabetes decreased mechanical threshold (mechanical allodynia) • Diabetes caused the first reduction and then a secondary increase in tail withdrawal and hot plate latency • Sodium nitrate preconditioning decreased the blood glucose and increased the serum insulin level in diabetic rats. • Sodium nitrate preconditioning reduced allodynia and thermal algesia in diabetic rats * Rana Keyhanmanesh

This study aimed to evaluate the effect of prolonged dietary nitrate supplementation on diabetic reproductive system.