Endocrine Abstracts

Introduction: Considering the protective effects nitrate has against diabetes and cardiovascular diseases, we aimed to determine effects of dietary nitrate on metabolic status and myocardial ischemia–reperfusion (IR) injury in type 2 diabetic rats.

Methods: Rats were divided into four groups (n=7): control, control+nitrate, diabetes, and diabetes+nitrate. Diabetes was induced by nicotinamide+streptozotocin, and nitrate added to drinking water (100 mg/l) of animals for 2 months. Serum nitrate+nitrite (NOx), glucose, lipid profile, total antioxidant capacity (TAC), catalase (CAT) activity, and systolic blood pressure (SBP) were measured before and after the study. After 2 months, i.v. glucose tolerance test was performed and hearts were perfused by Langendorff apparatus; before and after IR, LVDP, and ±dp/dt, and heart levels of malondialdehyde (MDA) and NOx were measured.

Results: Diabetic rats had lower serum NOx values compared to baseline (29.2±5.6 μmol/l vs 39.0±3.2 μmol/l, P<0.05), which normalized after nitrate therapy. Serum glucose in the diabetes+nitrate group was less increased, than the diabetes one (24.1% vs 90.2%; P<0.05). Nitrate therapy in diabetic rats significantly improved glucose tolerance and decreased serum cholesterol, LDL-C, and triglycerides by 22.9, 54.2, and 47.6% respectively and increased serum HDL-C by 42.4% compared to baseline. Diabetic rats had lower TAC and CAT activity, which normalized after dietary nitrate therapy. Recovery of LVDP and +dp/dt were 15 and 17% lower in diabetic rats vs controls respectively, but almost normalized after dietary nitrate, which also restored elevated SBP to near normal status (131.2±4.4 vs 120.6±2.2). Compared to controls, heart NOx level was lower in diabetic rats before IR, but was higher after. Diabetic rats had higher MDA levels both before and after IR, which along with heart NOx levels stabilized following dietary nitrate.

Conclusions: Nitrate therapy improved glucose tolerance, restored dyslipidaemia, prevented increase in SBP, and provided cardioprotection against IR injury in diabetic rats.

Disclosure: This work was supported by the Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences (grant numbers 498 and 711) and Department of Medical Laboratory Sciences, Faculty of Paramedical Sciences, Shahid Behesht.