Effect of tetrahydrobiopterin and exercise training on endothelium-dependent vasorelaxation in SHR.

We examined whether the improvement of impaired NO-dependent vasorelaxation by exercise training could be mediated through a BH4-dependent mechanism. Male spontaneously hypertensive rats (SHR, n = 20) and Wistar-Kyoto rats (WKY, n = 20) were trained (Tr) for 9 weeks on a treadmill and compared to age-matched sedentary animals (Sed). Endothelium-dependent vasorelaxation (EDV) was assessed with acetylcholine by measuring isometric tension in rings of femoral artery precontracted with 10(-5) M phenylephrine. EDV was impaired in SHR-Sed as compared to WKY-Sed (p = 0.02). Training alone improved EDV in both WKY (p = 0.01) and SHR (p = 0.0001). Moreover, EDV was not different in trained SHR than in trained WKY (p = 0.934). Pretreatment of rings with L-NAME (50 μM) cancelled the difference in ACh-induced relaxation between all groups, suggesting that NO pathway is involved in these differences. The presence of 10(-5) M BH4 in the organ bath significantly improved EDV for sedentary SHR (p = 0.030) but not WKY group (p = 0.815). Exercise training turned the beneficial effect of BH4 on SHR to impairment of ACh-induced vasorelaxation in both SHR-Tr (p = 0.01) and WKY-Tr groups (p = 0.04). These results suggest that beneficial effect of exercise training on endothelial function is due partly to a BH4-dependent mechanism in established hypertension.Journal Articleinfo:eu-repo/semantics/publishe

Effect of personalized moderate exercise training on Wistar rats fed with a fructose enriched water

Abstract Background Metabolic Syndrom has become a public health problem. It mainly results from the increased consumption of fat and sugar. In this context, the benefits of personalized moderate exercise training were investigated on a metabolic syndrome male wistar rat model food with fructose drinking water (20–25% w/v). Different markers including body weight, metabolic measurements, blood biochemistry related to metabolic syndrome complications have been evaluated. Methods Male Wistar rats were randomly allocated to 4 groups: control (sedentary (C, n = 8) and exercise trained (Ex, n = 8)), fructose fed (sedentary (FF, n = 8) and exercise trained fructose fed rats (ExFF, n = 10)). ExFF and Ex rats were trained at moderate intensity during the last 6 weeks of the 12 weeks-long protocol of fructose enriched water. Metabolic control was determined by measuring body weight, fasting blood glucose, HOMA 2-IR, HIRI, MISI, leptin, adiponectin, triglyceridemia and hepatic dysfunction. Results After 12 weeks of fructose enriched diet, rats displayed on elevated fasting glycaemia and insulin resistance. A reduced food intake, as well as increased body weight, total calorie intake and heart weight were also observed in FF group. Concerning biochemical markers, theoretical creatinine clearance, TG levels and ASAT/ALAT ratio were also affected, without hepatic steatosis. Six weeks of 300 min/week of moderate exercise training have significantly improved overweight, fasting glycaemia, HOMA 2-IR, MISI without modify HIRI. Exercise also decreased the plasma levels of leptin, adiponectin and the ratio leptin/adiponectin. Regarding liver function and dyslipidemia, the results were less clear as the effects of exercise and fructose-enriched water interact together, and, sometimes counteract each other. Conclusion Our results indicated that positive health effects were achieved through a personalized moderate training of 300 min per week (1 h/day and 5 days/week) for 6 weeks. Therefore, regular practice of aerobic physical exercise is an essential triggering factor to attenuate MetS disorders induced by excessive fructose consumption

Effect of exercise training on oxidative stress and mitochondrial function in rat heart and gastrocnemius muscle

International audienc

Metabolic Syndrome and Hypertension Resulting from Fructose Enriched Diet in Wistar Rats

Increased sugar consumption, especially fructose, is strongly related to the development of type 2 diabetes (T2D) and metabolic syndrome. The aim of this study was to evaluate long term effects of fructose supplementation on Wistar rats. Three-week-old male rats were randomly divided into 2 groups: control (C; n=14) and fructose fed (FF; n=18), with a fructose enriched drink (20–25% w/v fructose in water) for 21 weeks. Systolic blood pressure, fasting glycemia, and bodyweight were regularly measured. Glucose tolerance was evaluated three times using an oral glucose tolerance test. Insulin levels were measured concomitantly and insulin resistance markers were evaluated (HOMA 2-IR, Insulin Sensitivity Index for glycemia (ISI-gly)). Lipids profile was evaluated on plasma. This fructose supplementation resulted in the early induction of hypertension without renal failure (stable theoretical creatinine clearance) and in the progressive development of fasting hyperglycemia and insulin resistance (higher HOMA 2-IR, lower ISI-gly) without modification of glucose tolerance. FF rats presented dyslipidemia (higher plasma triglycerides) and early sign of liver malfunction (higher liver weight). Although abdominal fat weight was increased in FF rats, no significant overweight was found. In Wistar rats, 21 weeks of fructose supplementation induced a metabolic syndrome (hypertension, insulin resistance, and dyslipidemia) but not T2D

Progressive Induction of Type 2 Diabetes: Effects of a Reality–Like Fructose Enriched Diet in Young Wistar Rats

International audiencePurpose The aim of this study was to characterize short and medium-lasting effects of fructose sup-plementation on young Wistar rats. The diet was similar to actual human consumption. Methods Three week old male rats were randomly divided into 2 groups: control (C; n = 16), fructose fed (FF; n = 16) with a fructose enriched drink for 6 or 12 weeks. Bodyweight, fasting glyce-mia and systolic blood pressure were monitored. Glucose tolerance was evaluated using an oral glucose tolerance test. Insulinemia was measured concomitantly and enable us to calculate insulin resistance markers (HOMA-IR, Insulin Sensitivity Index for glycemia: ISI-gly). Blood chemistry analyses were performed. Results After six weeks of fructose supplementation, rats were not overweight but presented increased fasting glycemia, reduced glucose tolerance, and lower insulin sensitivity compared to control group. Systolic blood pressure and heart weight were also increased without any change in renal function (theoretical creatinine clearance). After twelve weeks of fructose supplementation, FF rats had increased bodyweight and presented insulin resistance (higher HOMA-IR, lower ISI-gly). Rats also presented higher heart volume and lower ASAT/ALAT ratio (presumed liver lesion). Surprisingly, the Total Cholesterol/Triglycerides ratio was increased only after six weeks of fructose supplementation, predicting a higher LDL presence and thus a higher risk of developing cardiovascular disease. This risk was no longer present after twelve weeks of a fructose enriched diet

Effects of fructose supplementation on bodyweight, fasting glycemia, theoretical creatinine clearance and plasma ASAT, ALAT, albumin and lipid levels.

<p>Effects of fructose supplementation on bodyweight, fasting glycemia, theoretical creatinine clearance and plasma ASAT, ALAT, albumin and lipid levels.</p

Effects of fructose supplementation on systolic blood pressure and heart volume.

<p>(3A) Systolic blood pressure was measure at age 8 weeks (<i>n = 8</i> for both FF and C). (3B) Heart volume was measured at age 9 and 15 weeks; at age 9 weeks <i>n = 8</i> for both C and FF rats, at age 15 weeks <i>n = 7</i> for both groups. FF: fructose supplemented; C: control. Statistical values: *<0.05, **<0.01, ***<0.001.</p

Effects of fructose supplementation on GPx, CAT and SOD activities in both left ventricle (LV) and gastrocnemius.

<p>(<i>n = 8</i> in all conditions).</p

Effects of fructose supplementation on Insulin Sensitivity Indices for glycemia (ISI-gly) and Homeostasis Model Assessment for Insulin Resistance (HOMA-IR).

<p>(2A) ISI-gly was calculated at both 9 and 13 weeks. (2B) HOMA-IR was calculated at both 9 and 13 weeks. FF: fructose supplemented; C: control. For both indicator: at age 9 weeks <i>n = 6</i> for both C and FF, at age 13 weeks <i>n = 7</i> for C rats and <i>n = 7</i> for FF rats. Statistical values: *<0.05, **<0.01, ***<0.001.</p