Biomedical subjects

S Rousseau-Migneron

Publications and source records attributed to S Rousseau-Migneron.

At least 19 recordsLinked to original sources

PubMed1992

Adrenodemedullation does not impair the beneficial effect of physical training in streptozotocin-diabetic rats.

This study was designed to ascertain if the improvement in glucose homeostasis found in diabetic animals submitted to physical training is due to an increased secretion of epinephrine by the adrenal medullae. Male Wistar rats were surgically adrenodemedullated (ADM group) or sham-operated (SHAM group). After a 3-week recovery period, a bolus of streptozotocin (40 mg/kg) was injected intravenously (IV), and the animals presenting 1 week later with a blood glucose value between 14 and 22 mmol/L were retained in the protocol and randomly assigned to a sedentary (SHAM-DS and ADM-DS) or trained (SHAM-DT and ADM-DT) group. Physical training was done on a treadmill according to a 10-week progressive program. An IV glucose tolerance test (0.5 g/kg) was performed in previously cannulated rats, 64 hours after the last bout of exercise. Pancreatic insulin and glucagon content was also determined. In sedentary diabetic rats, adrenodemedullation had no effect on plasma glucose, insulin, or glucagon levels, neither in the basal state nor following the glucose load. Basal glucose levels were diminished by training in both SHAM (16.1 +/- 1.5 v 21.8 +/- 0.4 mmol/L; P less than .01) and ADM (12.4 +/- 1.7 v 21.1 +/- 1.2 mmol/L; P less than .01) groups, with values lower in ADM-DT than in SHAM-DT rats (P less than .05). After glucose loading, the glucose levels were significantly lower (P less than .01) throughout the test in both SHAM-DT and ADM-DT rats than in their sedentary counterparts.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗

PubMed1992

Physical training increases beta-adrenoceptor density and adenylate cyclase activity in high-oxidative skeletal muscle of diabetic rats.

The effects of physical training on beta-adrenergic-receptor density (Bmax) and adenylate cyclase (AC) activity in soleus muscles (type I) and the deep red portion (type IIa) and superficial white portion (type IIb) of vastus lateralis muscles in diabetic rats were investigated. Rats were rendered diabetic with streptozotocin ([STZ] 45 mg/kg intravenously [IV]) and were either kept sedentary ([SD] n = 12) or submitted to a progressive 10-week treadmill running program ([TD] n = 13). A group of normal sedentary rats served as controls ([SC] n = 13). Plasma glucose levels were increased in SD rats in comparison with SC rats (21.3 +/- 1.4 mmol/L v 7.7 +/- 0.2; mean +/- SE, P < .001), but levels were partially reversed to normal by training (10.7 +/- 1.7; P < .01 v SD). The gastrocnemius nicotinamide adenine dinucleotide (NAD)-isocitrate dehydrogenase (ICDH) activity was significantly increased in TD rats in comparison to SC or SD rats (P < .001). The Bmax and antagonist affinity (Kd) determined with 125iodocyanopindolol (ICYP) were not affected by diabetes in any of the three types of muscle. In type I muscle, TD rats showed a significant 67% increase in Bmax compared with that of SD rats (TD 26.7 +/- 2.0 v SD 16.0 +/- 1.0; P < .001). In type IIa muscle, Bmax was significantly higher by 68% in TD rats as compared with SD rats (TD 16.5 +/- 1.7 v SD 9.8 +/- 0.9 fmol/mg protein; P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗

PubMed1992

Partial correction of impaired creatine kinase activity in diabetic rat heart by physical training.

The effect of physical training on total creatine kinase (CK), CK-MM, and CK-MB isoenzyme activity was studied in hearts of diabetic and control rats. Diabetes was induced with streptozotocin (50 mg/kg), and only rats with blood glucose levels between 14 and 22 mmol/L 1 week later were kept in the protocol. Exercise training was performed on a treadmill in a progressive 10-week program. Physical training did not induce any significant changes in plasma glucose or insulin levels in diabetic rats. Total CK, CK-MM, and CK-MB activity was decreased in diabetic rat heart by 27%, 22%, and 56%, respectively. Physical training did not induce any important changes in CK activity in heart of nondiabetic rats. However, in diabetic rat heart, training increased total CK activity by 13%, CK-MM activity by 12%, and CK-MB activity by 31%. We conclude that the decrease in cardiac CK activity observed in chronic experimental diabetes mellitus can be partly alleviated by a program of physical training. This may be one of the mechanisms whereby physical conditioning improves cardiac function in experimental diabetes.

Analysis of Variance↗

PubMed1991

Validation of the polyethylene glycol precipitation technique for the characterization of rat ventricular beta-adrenoceptors.

The use of polyethylene glycol (PEG) to separate [125I]cyanopindolol bound to rat ventricular membranes from free ligand in the characterization of beta-adrenoceptors was compared with the more frequently utilized filtration technique through GF/F glass-fiber filters. The results obtained in tissue from 14 rats demonstrated the following: (i) no significant difference between the two methods for the density of beta-adrenoceptors in ventricular tissue (PEG: 30.9 +/- 1.5 vs GF/F: 28.6 +/- 2.0 fmol/mg of protein); (ii) no significant difference for the dissociation constant (PEG: 70.7 +/- 5.3 vs GF/F: 57.7 +/- 7.7 pM); (iii) similar values for the Hill coefficient (PEG: 0.996 +/- 0.004 vs GF/F: 0.988 +/- .016); (iv) a significant difference for the relationship of bound/free vs bound, expressed as r2 (PEG: 0.82 +/- 0.03 vs GF/F: 0.74 +/- 0.03 P less than 0.05). The apparently greater accuracy of the PEG method over the filtration technique is probably explained by a lower degree of nonspecific binding observed with this method than with the filtration technique. In conclusion, the PEG precipitation method is an interesting and accurate alternative to the more standard filtration technique in ventricular beta-adrenoceptor characterization.

Animals↗

PubMed1991

Effect of physical training on ventricular beta-adrenergic receptor adenylate cyclase system of diabetic rats.

This study was designed to assess the effect of physical training on the ventricular beta-adrenergic receptor adenylate cyclase system of diabetic rats. Mild diabetes mellitus was induced by an intravenous (IV) injection of streptozotocin (45 mg/kg). Rats were randomized into a group submitted to a progressive 10-week running program on a treadmill, while another group was kept sedentary. A group of sedentary nondiabetic rats was used as normal controls. Results showed a similar reduction in the density of beta-adrenergic receptors in sedentary diabetic (P less than .05) and trained diabetic rats (P less than .01) compared with controls, without any significant alteration in the dissociation constant. The basal and the sodium fluoride-stimulated maximal adenylate cyclase activities were similar in the three groups. However, the maximal response of adenylate cyclase to isoproterenol was significantly reduced in the two diabetic groups compared with controls (P less than .01). The decrease in adenylate cyclase response to isoproterenol observed in the diabetic groups appeared to be associated with a reduction in the total number of beta-adrenergic receptors and more specifically in those existing in the high-affinity state. On the other hand, the hyperglycemia and hyperglucagonemia present in sedentary diabetic rats was improved by training. These data suggest that the beneficial effects observed in response to training in experimental diabetes are not associated with changes in beta-adrenergic receptor adenylate cyclase system on membranes from ventricular tissue.

Adenylyl Cyclases↗

PubMed1991

Plasma epinephrine in chronically adrenodemedullated rats: lack of response to acute or chronic exercise.

Even if it is well established that epinephrine is a hormone originating from the adrenal medullae, the reappearance of circulating epinephrine has been reported in rats a few days after adrenodemedullation. To verify if the extra-adrenal tissue responsible for this epinephrine production can be stimulated, sham-operated or adrenodemedullated rats, either trained or kept sedentary, were submitted to an acute exercise stimulation test. Blood sampling was done before and after the test in precannulated rats for the determination of plasma epinephrine, norepinephrine, and corticosterone levels. Basal epinephrine levels were significantly reduced in trained and sedentary adrenodemedullated rats compared with their sham-operated counterparts. In response to exercise, there was no significant rise in epinephrine levels in both groups of adrenodemedullated rats. The norepinephrine levels in the basal state and in response to exercise were not altered by adrenodemedullation nor by physical conditioning. Basal corticosterone levels were similar between adrenodemedullated and sham-operated animals, either trained or kept sedentary. In response to exercise, corticosterone levels increased significantly in each group of rats but to a lesser extent in both groups of adrenodemedullated animals. These data indicate that the extra-adrenal epinephrine secretion that develops in the absence of adrenal medullae is not influenced by acute exercise nor by physical training.

Adrenal Medulla↗

PubMed1991

Beta-adrenoceptor adenylate cyclase system adaptation to physical training in rat ventricular tissue.

The beta-adrenergic receptor adenylate cyclase system of ventricular tissue was evaluated in a group of rats submitted to a progressive 10-wk running program on a treadmill and compared with that in a group of rats maintained sedentary during the same period. Adequate training was confirmed by a 46% increase in the gastrocnemius isocitrate dehydrogenase activity in the trained group [1.50 +/- 0.04 vs. 1.03 +/- 0.06 (SE) pmol.g-1.min-1; P less than 0.01). Binding studies with [125I]iodocyanopindolol showed a 13% reduction in the density of beta-adrenergic receptors in trained rats (42.6 +/- 2.1 vs. 49.0 +/- 2.1 fmol/mg; P less than 0.05) without any significant modification in the dissociation constant. The amount of [125I]iodocyanopindolol bound to beta-adrenoceptors in the high-affinity state was reduced by 16.6% in trained rats (12.5 +/- 0.9 vs. 15.0 +/- 0.5 fmol/mg; P less than 0.05) without any significant changes for those in the low-affinity state, indicating a decrease in the coupling between the beta-adrenergic receptors and the guanine stimulatory binding protein. Furthermore, although the basal and sodium fluoride-stimulated adenylate cyclase activities were similar in the two groups of rats, the response of adenylate cyclase maximally stimulated by 10(-5) M isoproterenol was reduced by 16% in trained rats (29.7 +/- 1.4 vs. 35.3 +/- 1.3 pmol.mg-1.min-1; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1990

Beneficial effect of exercise training on cardiac long-chain acylcarnitine levels in diabetic rats.

Long-chain acylcarnitines are markedly elevated in the diabetic rat heart. This could be associated with the increased rate of fatty acid metabolism in this tissue seen in the diabetic animal. The effect of exercise training on this carnitine derivative in the diabetic rat, however, has received little attention. We therefore examined the effect of exercise training on this derivative as well as other carnitine esters in hearts of diabetic rats. Four groups of male Wistar rats were used: sedentary-control (SC), trained-control (TC), sedentary-diabetic (SD), and trained-diabetic (TD). Diabetes was induced by the I.V. injection of streptozotocin at the dose of 50 mg/kg. Training was performed on a motor-driven treadmill according to a 10-week program. Sixty hours after the last bout of exercise, the rats were killed by decapitation and the hearts were quickly excised and placed in liquid nitrogen for measurement of total carnitine and its acyl derivatives. SD and TD had significantly lower levels of total (p less than 0.001) and free carnitine (p less than 0.01) compared to the respective control groups. Exercise had no effect on total and free carnitine levels in both control and diabetic groups. Short-chain acylcarnitine levels were neither altered by training nor diabetes. Heart tissue levels of long-chain acylcarnitine were increased (p less than 0.01) in SD compared to SC. However, exercise training resulted in a significant (p less than 0.05) reduction in long-chain acylcarnitines in diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Acylation↗

PubMed1990

Beneficial effect of exercise training on cardiac long-chain acylcarnitine levels in diabetic rats.

Long-chain acylcarnitines are markedly elevated in the diabetic rat heart. This could be associated with the increased rate of fatty acid metabolism in this tissue seen in the diabetic animal. The effect of exercise training on this carnitine derivative in the diabetic rat, however, has received very little attention. We therefore examined the effect of exercise training on this derivative as well as other carnitine esters in hearts of diabetic rats. Four groups of male Wistar rats were used: sedentary-control (SC), trained-control (TC), sedentary-diabetic (SD), and trained-diabetic (TD). Diabetes was induced by the I.V. injection of streptozotocin at the dose of 50 mg/kg. Training was performed on a motor-driven treadmill according to a ten-week program. 60 hr after the last bout of exercise, the rats were killed by decapitation and the hearts were quickly excised and placed in liquid nitrogen for measurement of total carnitine and its acyl derivatives. SD and TD had significantly lower levels of total (p less than 0.001) and free carnitine (p less than 0.01) compared to the respective control groups. Exercise had no effect on total and free carnitine levels in both control and diabetic groups. Short-chain acylcarnitine levels were neither altered by training nor diabetes. Heart tissue levels of long-chain acylcarnitine were increased (p less than 0.01) in SD compared to SC. However, exercise training resulted in a significant (p less than 0.05) reduction in long-chain acylcarnitines in diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Acylation↗

PubMed1990

Physical training of moderate intensity improves survival rate of diabetic rats submitted to experimental myocardial infarction.

The present study was designed to compare the effect of three programs of exercise of different intensity on the survival rate of normal and streptozotocin-diabetic rats (60 mg/kg) submitted to acute experimental myocardial infarction. The animals were trained progressively on a treadmill once a day, five days per week for eight weeks at a 10 degree incline according to one of the following treadmill running programs: light (30 mins/day at 20 m/min), moderate (30 mins/day at 25 m/min) or heavy (60 mins/day at 25 m/min). Myocardial infarction was produced by left coronary artery ligation under ether anesthesia three days after the last bout of exercise. Successful ligation was demonstrated by elevated plasma creatine kinase MB isoenzyme levels 4 h later or by dye injection in rats with early death. In sedentary diabetic rats (n = 33), the early survival rate was decreased in comparison to sedentary controls (n = 22), although statistical significance was not reached, (30 versus 45%; P = 0.1952 by Fisher's exact test). These values were not significantly modified by light or heavy training in control (light n = 18, 61%; heavy n = 25, 56%) nor in diabetic animals (light n = 28, 32%; heavy n = 23, 39%). While the survival rate was not altered by moderate exercise in control animals (n = 26, 62%), it was greatly improved in diabetic rats (n = 23, 64%, P = 0.0108 versus sedentary diabetics). These data suggest that it is possible to improve the early survival rate of diabetic rats submitted to experimental myocardial infarction by a previous training program at a moderate level of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Diminished hypotensive response to isoproterenol in streptozotocin-diabetic rats.

1. The cardiovascular reactivity of streptozotocin-diabetic rats has been evaluated with isoproterenol (ISO), a strong beta-adrenergic agonist able to produce, at large dose, myocardial infarction. 2. In the basal state, diabetic rats presented significantly lower heart rate (P less than 0.001), a decreased systolic (P less than 0.05) and an unaltered diastolic blood pressure compared to non-diabetics. 3. Following ISO stimulation, the chronotropic response was similar in both groups of rats, while the fall in systolic and diastolic pressure was markedly reduced compared to those of non-diabetic rats (P less than 0.001). 4. These results suggest that the vasodilation capacity of diabetic rats is diminished.

Animals↗

PubMed1988

Exercise training improves early survival rate in diabetic rats submitted to acute coronary artery ligation.

This study was designed to test the hypothesis that the decreased early survival rate of diabetic rats submitted to acute experimental myocardial infarction could be improved by a previous training program. Male Wistar rats (+/- 200 g) were rendered diabetic with the i.v. injection of streptozotocin (45 mg/kg) but only those presenting one week later a tail-blood glucose value between 250-400 mg/dl were retained in the protocol. Diabetic and control rats were either kept sedentary or submitted to a progressive 10-week program of treadmill running. The left coronary artery was then ligated under ether anesthesia. Adequate occlusion was confirmed by an elevation of plasma CK-MB levels four hours later or by a toluidine blue injection technique in rats which died earlier. Since the first 20 minutes after such a procedure represents a most critical period for sudden death, the early survival rate was calculated for each group of rats and significance in differences was established with the Fisher's test. While the 27% early survival rate observed in sedentary diabetics was significantly lower (p = 0.02) than the 49% found in sedentary controls, this was completely alleviated by previous training in diabetic animals (50%; p = 0.018 vs sedentary diabetics and 0.623 vs sedentary controls). This beneficial effect of training was not found in nondiabetic animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Transient increase in basal insulin levels in severely diabetic rats submitted to physical training.

Physical training improves glucose homeostasis in rats with experimental diabetes mellitus. The present study has been designed to ascertain if this beneficial effect is maintained or lost after a few days of inactivity. Male Wistar rats were injected with streptozotocin (STZ, 50 mg/kg) and those presenting one week later a blood glucose value between 250 and 400 mg/dl were retained in the protocol and randomly assigned to a sedentary (n = 18) or trained group (n = 23). An I.V. glucose tolerance test (0.5 g/kg) was performed in previously cannulated rats 64 h (trained rats; n = 15) or 12 days (detrained rats, n = 8) after the last bout of exercise. In comparison with results obtained in their sedentary counterparts (419 +/- 15 mg/dl), basal glucose levels were significantly lower in trained (362 +/- 20; p less than 0.05), but not in detrained rats (429 +/- 15; NS). Similar differences in plasma glucose levels were observed after glucose loading, even though the glucose disappearance rate constant was not significantly improved by training. Furthermore, basal insulin levels were significantly higher (p less than 0.01) in trained than in sedentary rats (20 +/- 3 vs 12 +/- 2 microU/ml) but such a difference had disappeared in detrained rats (9 +/- 2 microU/ml). These results indicate that the training-induced improvement in glucose homeostasis of diabetic rats is a transient phenomenon which is associated with an increase in circulating insulin levels. This suggests that the beneficial effect of training is not due solely to enhanced insulin sensitivity.

Animals↗

PubMed1987

Acute diabetes mellitus does not impair survival rate in rats submitted to left coronary artery ligation.

This study was designed to assess whether the acute metabolic disturbances associated with diabetes mellitus of three-days duration could influence the survival of rats submitted to experimental myocardial infarction. Diabetes was induced with streptozotocin (50 mg/kg) in male Wistar rats and three days later left coronary artery ligation was performed in both control (n = 34) and diabetic (n = 31) animals. Diabetic rats had significant alterations in plasma levels of glucose (424 +/- 6 vs 143 +/- 3 mg/dL; p less than 0.001), insulin (10 +/- 1 vs 32 +/- 2 microU/mL; p less than 0.001) and free carnitine (37 +/- 2 vs 52 +/- 2 microM; p less than 0.001). There was no significant difference in the survival rate of diabetic animals, either early after coronary artery ligation (32 vs 42% at 20 min; p greater than 0.1) or later (21 vs 25% at 1 week; p greater than 0.1). This suggests that the increased mortality rate found in diabetic subjects suffering from myocardial infarction is due to some long-term changes associated with chronic diabetes mellitus rather than to the acute metabolic disturbances present at the time of this event.

Acute Disease↗

PubMed1986

Effect of physical training on norepinephrine turnover in tissues of normal and diabetic rats.

This study was designed to examine the influence of physical training on the norepinephrine turnover rate in heart, pancreas, liver, and gastrocnemius muscles of normal and diabetic male rats at rest. Diabetes was induced with the IV injection of streptozotocin (45 mg/kg) and physical training was done on a treadmill according to a ten-week program. Norepinephrine turnover rate of tissues was estimated by following over time the decay in the specific activity of norepinephrine after a single IV bolus of tritiated norepinephrine (30 microCi/kg). Plasma glucose, insulin, and glucagon levels were also measured at the time of death. Although training caused a reduction in the plasma glucose values of diabetic rats, no changes in norepinephrine turnover rate were observed after the conditioning program. On the other hand, diabetes was associated with a significant 30% to 40% decrease in the pancreatic norepinephrine turnover rate. It is concluded that the beneficial effects of physical training on diabetes mellitus cannot be explained by adaptive changes in the sympathetic nervous system activity and that further work will be necessary to elucidate the mechanism whereby streptozotocin diabetes diminishes the pancreatic norepinephrine turnover.

Animals↗

PubMed1986

Increased mortality rate in diabetic rats submitted to acute experimental myocardial infarction.

Diabetes mellitus is well known to increase the death rate after acute myocardial infarction in humans. The mechanisms of this adverse effect of diabetes, however, remain unknown. In the present study an animal model was developed in which the influence of diabetes on the survival rate after acute myocardial infarction could be studied in more detail. Male Wistar rats were rendered diabetic with streptozotocin (45 mg X kg-1 intravenously) and kept in the study if one week later their tail blood glucose concentration was between 13.9 and 22.2 mmol X litre-1 after a four hour fast. Ten weeks later they underwent acute left coronary artery ligation. In comparison with control rats (n = 30), diabetic rats (n = 32) had a higher mortality in the first 20 minutes after acute coronary artery ligation (78% vs 53%; p less than 0.05 by chi 2 test). Creatine kinase-MB isoenzyme activity tended to increase less in surviving diabetic rats than in their non-diabetic counterparts. Moreover, blood samples collected a few minutes before the surgical procedure showed that diabetic rats dying within the first 20 minutes (n = 25) had higher mean (SEM) plasma glucose concentrations (26.9(0.5) vs 23.4(1.2) mmol X litre-1; p less than 0.01) and lower mean(SEM) plasma insulin concentrations (20(1) vs 26(2) mU X litre-1; p less than 0.05) than those (n = 7) that survived that critical period.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Hyperglycemic effect of high doses of dobutamine in the rat: studies of insulin and glucagon secretion.

The influence of dobutamine on glucoregulation has been assessed in the rat during and after an intravenous infusion given at the following doses: 0, 0.1, 1.0, 10, 100, and 1000 micrograms X kg-1 X min-1. Plasma glucose, insulin, and glucagon levels were measured at 15-min intervals in unanesthetized previously cannulated rats. Basal glucose levels were preserved with the less than or equal to 10 micrograms X kg-1 X min-1 doses. At the greater than or equal to 100 micrograms X kg-1 X min-1 doses, a marked hyperglycemic effect was observed, partly attributable to some inhibitory effect of dobutamine on glucose-induced insulin secretion and to its stimulatory effect on glucagon secretion. Such data suggest that dobutamine may disturb the normal glucose homeostasis, particularly in situations of deficient insulin reserve.

Animals↗

PubMed1985

Diminished glucagon response to epinephrine in physically trained diabetic rats.

The effect of physical training on glucose, insulin, and glucagon response to epinephrine was assessed in normal and diabetic rats. Male Wistar rats were injected with streptozocin (STZ, 45 mg/kg) and those presenting 1 wk later a blood glucose value between 250 and 400 mg/dl were retained in the protocol and randomly assigned to a sedentary or trained group. Similar studies were conducted in control animals. Physical training was done on a treadmill according to a 10-wk program. Epinephrine (0.75 microgram/kg/min) was infused intravenously (i.v.) in previously cannulated rats for 1 h and arterial blood samples obtained at 15-min intervals for glucose, insulin, and glucagon measurements. Pancreatic insulin and glucagon content was also determined. Basal glucose levels were significantly lower in trained than in sedentary diabetic rats (P less than 0.01). The hyperglycemic response to epinephrine was diminished by 19% and 23% in trained control and diabetic animals, respectively, with a faster return to baseline after stopping epinephrine infusion in both trained groups. Although in nondiabetic rats this could be related to some diminution in the suppressive effect of epinephrine on insulin secretion, this was not the case in diabetic animals. Moreover, while training did not modify epinephrine-induced glucagon response in control rats, the twofold greater (P less than 0.01) glucagon response observed in sedentary diabetic rats was restored to normal in trained diabetic rats. After stopping epinephrine infusion, glucagon levels dropped below the baseline in both groups of trained rats but not in their sedentary counterparts. These effects of training on glucagon response could not be explained by changes in pancreatic glucagon content.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗