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S Rousseau-Migneron

Publications and source records attributed to S Rousseau-Migneron.

33 records · Page 2Linked to original sources
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↗
PubMed1985

Plasma, adrenal, and heart catecholamines in physically trained normal and diabetic rats.

This study was designed to evaluate the possibility that the enhanced insulin sensitivity of physically trained normal and diabetic rats is due to adaptive changes in the adrenergic system. Mild diabetes mellitus was induced in male Wistar rats with streptozocin (STZ, 45 mg/kg i.v.) and a 10-wk conditioning program was conducted by having the animals run on a treadmill. Rats were cannulated 16 h after the last period of exercise and blood sampling was obtained 48 h later for basal plasma glucose, insulin, epinephrine, and norepinephrine determination. Catecholamine measurements were also made in adrenals, atria, and ventricles from sedentary control, trained control, sedentary diabetic, and trained diabetic rats. The previously reported beneficial effect of physical training on diabetes mellitus was reproduced. While diabetes mellitus did not modify the catecholamine levels, the training program provoked an increase in plasma epinephrine concentrations, with a concomitant significant rise in adrenal epinephrine content. In heart tissue, the epinephrine values also tended to be increased by training although statistical significance was not reached. These data suggest that basal secretion of epinephrine is somewhat increased in trained rats. Whether this may trigger adaptive changes that could be involved in the beneficial effect of physical training on experimental diabetes mellitus remains to be elucidated.

Adrenal Glands↗
PubMed1983

Long-term changes in the diabetic state induced by different doses of streptozotocin in rats.

The long-term effects of different doses (0, 25, 35, 45, 55, 65 and 100 mg/kg) of streptozotocin (STZ) in male Wistar rats had been followed over a 16 week period. The weight-gain curve and the epididymal fat pad weight were significantly different (P less than 0.05) from control after 1 week with the 65 and 100 mg/kg doses and after 4 weeks with the 45 and 55 mg/kg doses; there were no significant changes with the 25 and 35 mg/kg doses even after 16 weeks. An i.v. glucose tolerance test (0.5 g/kg) was performed at 1, 4 or 16 weeks after the injection of STZ. The basal levels of glucose were significantly elevated (P less than 0.05) after 1 week with the greater than or equal to 55 mg/kg doses, and after 16 weeks with the greater than or equal to 45 mg/kg doses; there was also an overall increase in the basal glucose levels between 1 and 16 weeks in rats treated with the greater than or equal to 45 mg/kg doses. The basal insulin levels were significantly decreased (P less than 0.05) after 1 week with the greater than or equal to 65 mg/kg doses, after 4 weeks with the greater than or equal to 55 mg/kg doses and after 16 weeks with the greater than or equal to 35 mg/kg doses. The insulin peak 2 min after the glucose load was significantly less (P less than 0.05) after 1 week with the greater than or equal to 35 mg/kg doses and after 16 weeks with the greater than or equal to 25 mg/kg doses. The use of an insulinogenic index to assess the insulin secretory capacity showed a significant decrease (P less than 0.05) for the greater than or equal to 35 mg/kg doses at each tested time; with the 45 mg/kg dose, there was a further significant decrease (P less than 0.01) between the first and sixteenth week. The present long-term studies showed that there is a progressive deterioration in the glucose tolerance and insulin secretion after the injection of different doses of STZ. Furthermore, changes in glucose-insulin interrelationships over time suggest that the insulin insensitivity previously described in STZ diabetic rats might be only an early transient phenomenon.

Adipose Tissue↗
PubMed1982

Effects of physical training on beta-adrenergic receptors in rat myocardial tissue.

A diminished sympathetic activity has been related to training bradycardia seen at rest and during exercise. In order to evaluate if changes in heart adrenergic receptors can be one of the mechanisms by which the sympathetic responsiveness could be decreased by physical training, the number and affinity of beta-adrenergic receptors were determined in heart ventricular tissue of rats submitted to a 10-week running programme. Binding studies were done at different concentrations of (-)[3H] dihydroalprenolol (DHA) (0.5 to 14.4 nmol X litre-1) with ventricular membrane preparations from control and trained rats. Direct linear plot analysis revealed that physical training reduced the total number (1933 +/- 192 vs 2922 +/- 211 fmol X ventricles-1; P less than 0.01) density of beta-adrenergic receptors expressed either as fmol X mg-1 of membrane protein (34 +/- 3 vs 43 +/- 3; P less than 0.05) or as fmol X g-1 ventricle (1740 +/- 170 vs 2308 +/- 155; P less than 0.05). There was no significant change in the dissociation constant (3.11 +/- 0.14 vs 4.08 +/- 0.51 nmol X litre-1; P greater than 0.05). Basal plasma noradrenaline levels were not affected by training (116 +/- 18 vs 101 +/- 14 pg X cm-3; P greater than 0.10); however the adrenaline values were significantly higher in trained rats (91 +/- 16 vs 47 +/- 7 pg X cm-3; P less than 0.05). These data indicate that physical training induces changes at the level of beta-adrenergic receptors and this may partly explain the bradycardia seen in trained subjects and animals.

Animals↗
PubMed1982

Beneficial effects of physical training in rats with a mild streptozotocin-induced diabetes mellitus.

The present studies have been designed to evaluate the effects of physical training in rats with a diminished insulin reserve. Mild diabetes mellitus was induced in rats with 45 mg/kg streptozotocin. Physical training was done on a treadmill, with a progressive program, twice daily, 5 days per week, for 10 wk in control and diabetic rats. At the end of the training program, a significant diminution in body weight gain and in epididymal fat pad weight was observed in both trained groups, as compared with sedentary controls. Sixty-four hours after the last exercise, control (N = 16), control-trained (N = 14), diabetic (N = 17), and diabetic-trained (N = 15) rats were submitted to an intravenous glucose tolerance test (0.5 g/kg). Arterial blood samples were collected at -15, 0, 2, 4, 6, 10, 15, 30, 45, and 60 min during the test in unanesthetized and precannulated rats for plasma glucose and insulin determinations. In normal rats, physical training induced a sharp decrease in the basal insulin levels (36 +/- vs. 101 +/- 6 microunits/ml; P less than 0.001) without any significant changes in glucose levels (122 +/- 4 vs. 129 +/- 2 mg/dl; P less than 0.05). After the glucose loading there was no significant change in the glucose tolerance curve, although the insulin values remained lower throughout the test in the trained group. In the diabetic rats, the elevated basal glucose levels were significantly diminished in the trained group as compared with the untrained diabetic group (177 +/- 22 vs. 306 +/- 37 mg/dl; P less than 0.001), although the basal insulin values were similar in both groups (51 +/- 7 vs. 54 +/- 9 microunits/ml; P greater than 0.05). The improvement in the glucose tolerance of the diabetic-trained rats was further confirmed by the glucose disappearance rate constant that was significantly increased (3.6 0.4 vs. 2.0 +/- 0.3; P less than 0.01), although not fully restored to normal (6.3 +/- 0.2; P less than 0.001). These data clearly show that in rats with a diminished insulin reserve, a 10-wk running program greatly improved the glucose homeostasis. Measurements of circulating insulin suggest that, although an effect on insulin secretion cannot be totally excluded, the beneficial effect of physical training on diabetes mellitus is probably best explained by an increase in insulin sensitivity.

Animals↗
PubMed1979

Effects of physical training and adiposity on glucose metabolism and 125I-insulin binding.

Eighteen young male subjects, aged 18-30 yr, with maximal oxygen intake (VO2max) varying between 36 and 80 ml.kg-1.min-1, were studied. Between 20 and 120 min after injection, tolerance to iv glucose (20 g/m2) was not affected by VO2max but the insulin response was very significantly reduced in the better trained subjects. 125I-insulin binding to monocytes was found to be greater in the best trained subjects. Simple correlation analysis indicates that both VO2max and adiposity are related to plasma glucose and plasma insulin levels as well as to 125I-insulin binding. Because VO2max is negatively correlated to percent of body fat, a partial correlation analysis was made. Results indicate that the differences observed in athletes with regard to glucose and insulin levels and 125I-insulin binding are related to reduced adiposity rather than to enhanced VO2max.

Adipose Tissue↗
PubMed1977

Metabolic and cardiovascular responses to norepinephrine in trained and nontrained human subjects.

Forty young male adults, aged 18-30 yr, with maximal oxygen intake (VO2 max) varying between 35 and 76 ml-kg-1-min-1 were studied. The fasting subjects were perfused for 15 min with saline and thereafter for 30 min with norepinephrine (0.1 mug/kg per min). Blood variables were determined at the end of slaine perfusion, at 15 and 30 min during norepinephrine perfusion and 15 min after the end of NE perfusion. Trained subjects are characterized by lower basal plasma glucose and insulin concentration. NE perfusion produced a larger increase in plasma glucose in the trained subjects. Levels of insulin in the postperfusion period were smaller in the trained group. Serum free fatty acids (FFA) and glycerol increased less in the trained subjects during NE perfusion and this difference persisted in the post-perfusion period. During NE perfusion, blood lactate increased only in the nontrained subjects. Initial heart rate and blood pressure were lower in trained subjects but, during NE perfusion, elevated levels of blood pressure and decreased levels of heart rate were comparable in both groups. Because of similarities in responses to exercise and to NE in trained subjects, the results of the present study suggest a possible role for NE in exercise training.

Adolescent↗
PubMed1976

Effect of adrenaline on insulin secretion in rats treated chronically with adrenaline.

To determine whether rats could adapt to a chronic exogenous supply of adrenaline by a decrease in the well-known inhibitory effect of adrenaline on insulin secretion, plasma glucose and insulin levels were measured in unanesthetized control and adrenaline-treated rats (300 mug/kg twice a day for 28 days) during an adrenaline infusion (0.75 mug kg-1 min-1), after an acute glucose load (0.5 g/kg), and during the simultaneous administration of both agents. Chronic treatment with adrenaline did not modify the initial glucose levels but it greatly diminished the basal insulin values (21.57+/-2.48 vs. 44.69+/-3.3muU/ml, p less than 0.01). In the control rats, despite the elevated glucose concentrations, a significant drop in plasma insulin levels was observed within the first 15 min of adrenaline infusion, followed by a period of recovery. In the adrenaline-treated group, in which plasma glucose levels were lower than in control animals, plasma insulin levels did not drop as in control rats, but a significant increase was found after 30 min of infusion. During the intravenous glucose tolerance test, the plasma glucose and insulin responses showed similar patterns; however, during the concomitant adrenaline infusion, the treated rats showed a better glucose tolerance than their controls. These results indicate that rats chronically treated with adrenaline adapt to the diabetogenic effect of an infusion of adrenaline by have a lower inhibition of insulin release, although the lower basal insulin levels may indicate a greater sensitivity to endogenous insulin.

Animals↗
PubMed1975

Effects of adrenaline on the dynamics of carbohydrate metabolism in rats treated chronically with adrenaline.

Following a subcutaneous injection of adrenaline (300 mug/kg), blood-glucose levels were lower in rats treated chronically with adrenaline (300 mug/kg twice a day for 28 days) than in control rats during at least 2.5 h after the injection. To explain this difference of response, the turnover rate of glucose was measured in control and adrenaline-treated rats during adrenaline infusion (0.75 mug/kg- minus 1 min- minus 1), with [U- minus 14C]glucose as tracer. It was found that the rate of appearance of glucose was greater in the control than in the adrenaline-treated group after a 120-min infusion of adrenaline. The rate of disappearance of glucose in the treated rats increased during the first 60 min of infusion and stayed at this elevated level for a subsequent 2 h, whereas in the control rats, it remained unchanged at the beginning of adrenaline infusion and significantly increased only during the second and third hours of infusion. In addition, the metabolic- clearance rate of glucose was not modified by adrenaline in the treated group, but in the control group, the initial clearance rate was significantly less than in the treated group, and decreased during the first hour of adrenaline infusion even though blood glucose reached values of 244 mg/100 ml. ,rom these data, it is suggested that rats adapt to a chronic exogenous supply of adrenaline by a reduced increase in glucose production in response to adrenaline infusion and a better glucose utilization, which possibly indicates a decrease in the inhibitory effect of adrenaline on insulin secretion.

Animals↗
PubMedDate not supplied

Lidocaine improves survival rate in diabetic rats submitted to acute left coronary artery ligation.

This study was designed to evaluate whether the decreased early survival rate of diabetic rats submitted to acute experimental myocardial infarction can be improved by pretreatment with lidocaine. Male Wistar rats (+/- 210 g) were rendered diabetic with i.v. injection of streptozotocin (50 mg/kg), and only those presenting 1 week later a tail-blood glucose value between 250-400 mg/dl were retained in the protocol. Eleven weeks after induction of diabetes, a bolus of lidocaine (2 mg/kg) was administered i.v. about 6 min prior to ligation of the left coronary artery under ether anesthesia in control (n = 54) and diabetic (n = 48) rats; similar studies were conducted in 53 control and 55 diabetic rats without lidocaine pretreatment. Adequate occlusion was confirmed by an elevation of plasma CK-MB levels 4 h later or by a toluidine blue injection technique in rats which died earlier. Rats were followed over 48 h and comparison in the survival rate in each group established with the Fisher's exact test. Early survival rate (measured after 20 min) was significantly decreased in diabetic rats (27% vs 45%; p = 0.04). This was greatly improved by lidocaine pretreatment in diabetic (60% vs 27%; p = 0.0013), but not in control animals (50% vs 45%; p = 0.348). Furthermore, the beneficial effect of prophylactic lidocaine observed early after coronary ligation in diabetic rats was maintained throughout the period of observation (48 h). These data suggest that the prophylactic use of lidocaine is able to reverse the increased incidence of sudden death following experimental myocardial infarction in chronically diabetic rats.

Animals↗
PubMedDate not supplied

Decrease in ventricular beta-adrenergic receptors in trained diabetic rats.

The effects of physical training on beta-adrenergic receptors were evaluated in heart ventricular tissue of diabetic rats. Mild diabetes mellitus was induced in rats with streptozotocin (45 mg/kg, iv). They were then submitted to a progressive 10-week running programme on a treadmill. Binding studies were done at six different concentrations of (-) [3H]dihydroalprenolol (0.5 to 14.4 nM) with ventricular membrane preparations from control (n = 13), sedentary diabetic (n = 9) and trained diabetic rats (n = 10). Direct linear plot analysis of the data revealed that the total number of beta-adrenoceptors was reduced in sedentary diabetic rats as compared to control (2231 +/- 207 vs 2922 +/- 211 fmol/ventricles; P less than 0.05); however, there was no significant change in the receptor density expressed as fmol/mg of membrane protein (40 +/- 3 vs 43 +/- 3; P greater than 0.05). On the other hand, the beta-adrenergic binding sites were decreased in training diabetic rats, either expressed as the total number of receptors (1920 +/- 179 vs 2922 +/- 211; P less than 0.01), or as fmol/mg of membrane protein (30 +/- 3 vs 43 +/- 3; P less than 0.01). There was no significant change in the dissociation constant (KD) of these receptors between groups (KD = 4.08 +/- 0.51, 4.69 +/- 0.93 and 2.88 +/- 0.39 nM respectively for control, sedentary diabetic and diabetic trained animals). The basal epinephrine concentration was significantly increased in trained diabetic rats (102 +/- 21 pg/ml vs 47 +/- 7 for control (P less than 0.05) and vs 49 +/- 9 for sedentary diabetic (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗