Abstract
BackgroundThe majority of studies have investigated the effect of exercise training (TR) on vascular responses in diabetic animals (DB), but none evaluated nitric oxide (NO) and advanced glycation end products (AGEs) formation associated with oxidant and antioxidant activities in femoral and coronary arteries from trained diabetic rats. Our hypothesis was that 8-week TR would alter AGEs levels in type 1 diabetic rats ameliorating vascular responsiveness.Methodology/Principal FindingsMale Wistar rats were divided into control sedentary (C/SD), sedentary diabetic (SD/DB), and trained diabetic (TR/DB). DB was induced by streptozotocin (i.p.: 60 mg/kg). TR was performed for 60 min per day, 5 days/week, during 8 weeks. Concentration-response curves to acetylcholine (ACh), sodium nitroprusside (SNP), phenylephrine (PHE) and tromboxane analog (U46619) were obtained. The protein expressions of eNOS, receptor for AGEs (RAGE), Cu/Zn-SOD and Mn-SOD were analyzed. Tissues NO production and reactive oxygen species (ROS) generation were evaluated. Plasma nitrate/nitrite (NOx −), superoxide dismutase (SOD), catalase (CAT), thiobarbituric acid reactive substances (TBARS) and Nε-(carboxymethyl) lysine (CML, AGE biomarker). A rightward shift in the concentration-response curves to ACh was observed in femoral and coronary arteries from SD/DB that was accompanied by an increase in TBARS and CML levels. Decreased in the eNOS expression, tissues NO production and NOx − levels were associated with increased ROS generation. A positive interaction between the beneficial effect of TR on the relaxing responses to ACh and the reduction in TBARS and CML levels were observed without changing in antioxidant activities. The eNOS protein expression, tissues NO production and ROS generation were fully re-established in TR/DB, but plasma NOx − levels were partially restored.ConclusionShear stress induced by TR fully restores the eNOS/NO pathway in both preparations from non-treated diabetic rats, however, a massive production of AGEs still affecting relaxing responses possibly involving other endothelium-dependent vasodilator agents, mainly in coronary artery.
Highlights
Exercise training is positively associated with better prognostic outcomes of certain chronic pathological conditions such as arterial hypertension, dyslipidemia, diabetes mellitus and obesity [1,2]
Shear stress induced by TR fully restores the endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) pathway in both preparations from non-treated diabetic rats, a massive production of advanced glycation end products (AGEs) still affecting relaxing responses possibly involving other endotheliumdependent vasodilator agents, mainly in coronary artery
Type 1 and type 2 diabetes mellitus are cardiometabolic diseases characterized by chronic hyperglycemia which has been associated with severe tissue damage resulting in long-term clinical outcomes such as kidney disease, retinopathy, vascular and neuron defects that result in foot problems and cardiovascular diseases [9,10,11,12]
Summary
Exercise training is positively associated with better prognostic outcomes of certain chronic pathological conditions such as arterial hypertension, dyslipidemia, diabetes mellitus and obesity [1,2]. Type 1 and type 2 diabetes mellitus are cardiometabolic diseases characterized by chronic hyperglycemia which has been associated with severe tissue damage resulting in long-term clinical outcomes such as kidney disease, retinopathy, vascular and neuron defects that result in foot problems and cardiovascular diseases [9,10,11,12]. Persistent hyperglycemia in both types of diabetes mellitus can activate alternative glucose metabolism pathways that in turn result in the formation of deleterious products derived from protein or lipid structure alterations named advanced glycation end products (AGEs) [13,14]. Our hypothesis was that 8week TR would alter AGEs levels in type 1 diabetic rats ameliorating vascular responsiveness
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