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Biomedical subjects

A Nadeau

Publications and source records attributed to A Nadeau.

At least 181 records · Page 10Linked to original sources

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↗

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↗

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↗

Effect of streptozotocin-induced diabetes on insulin binding parameters in adult rat testis.

Insulin binding parameters have been measured in testicular membranes of streptozotocin diabetic male rats. Insulin binding decrease was ascribed to the well-known depressing effect of diabetes mellitus on circulating luteinizing hormone (LH). Because both LH and insulin receptors are modulated by pituitary LH and because of their reduction in testes of diabetic rats, we conclude that Leydig cell dysfunction is a secondary disorder associated with this complex metabolic condition.

Animals↗

Regional distribution of body fat, plasma lipoproteins, and cardiovascular disease.

Several epidemiological studies have reported that the regional distribution of body fat is a significant and independent risk factor for cardiovascular disease (CVD) and related mortality. Although these associations are well established, the causal mechanisms are not fully understood. Numerous studies have, however, shown that specific topographic features of adipose tissue are associated with metabolic complications that are considered as risk factors for CVD such as insulin resistance, hyperinsulinemia, glucose intolerance and type II diabetes mellitus, hypertension, and changes in the concentration of plasma lipids and lipoproteins. The present article summarizes the evidence on the metabolic correlates of body fat distribution. Potential mechanisms for the association between body fat distribution, metabolic complications, and CVD are reviewed, with an emphasis on plasma lipoprotein levels and plasma lipid transport. From the evidence available, it seems likely that subjects with visceral obesity represent the subgroup of obese individuals with the highest risk for CVD. Although body fat distribution is now considered as a more significant risk factor for CVD and related death rate than obesity per se, further research is clearly needed to identify the determinants of body fat distribution and the causal mechanisms involved in the metabolic alterations. It appears certain, however, that an altered plasma lipid transport is a significant component of the relation between body fat distribution and CVD.

Abdomen↗

Heredity and changes in plasma lipids and lipoproteins after short-term exercise training in men.

The aims of this controlled experiment were to investigate the effects of short-term aerobic exercise training on plasma lipid and lipoprotein concentrations and the role of heredity in determining the individual variation observed in the lipoprotein-lipid response. Six pairs of male monozygotic (MZ) twins were subjected to an exercise training program that induced a 22,000 kcal energy deficit after 22 consecutive days of training. This program significantly reduced body weight, percent body fat, and subcutaneous fat and significantly increased maximal oxygen consumption (VO2max) (p less than 0.005). The plasma insulin response to an oral glucose challenge was markedly reduced after training (p less than 0.001). Plasma triglyceride concentration decreased and the high density lipoprotein cholesterol (HDL-CHOL)/CHOL ratio increased with training (p less than 0.05). Subjects also displayed substantial individual variation in their response to exercise training, but the changes in plasma CHOL, apolipoprotein (apo) B low density lipoprotein cholesterol (LDL-CHOL), HDL-CHOL, and the HDL-CHOL/CHOL ratio tended to be similar within MZ twin pairs (0.67 less than or equal to ri less than or equal to 0.92; 0.05 greater than p less than 0.0001) thus indicating a significant effect of heredity on the sensitivity of plasma lipids and lipoproteins to exercise training.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Adipose tissue distribution and plasma lipoprotein levels in obese women. Importance of intra-abdominal fat.

Prospective studies have shown that excess abdominal fat is associated with an increased risk of coronary heart disease and related death. We used computed axial tomography (CAT) to assess the association between deep and subcutaneous abdominal adipose tissue and plasma lipoprotein levels in a sample of 52 premenopausal obese women aged 35.7 +/- 5.5 years (mean +/- SD). Whereas the plasma lipoprotein concentration were not significantly correlated with fat mass, the data obtained by CAT indicated that the absolute amount of deep abdominal fat was negatively correlated with high density lipoprotein cholesterol (HDL-CHOL) levels (r = -0.35, p less than 0.01), as well as with HDL-CHOL/low density lipoprotein (LDL)-CHOL, HDL-apoprotein-(apo) A-I/LDL-apo B, and HDL2-CHOL/HDL3-CHOL ratios (-0.32 less than or equal to r less than or equal to -0.40, 0.05 greater than p less than 0.01). Adipose tissue deposition at the mid-thigh region determined by CAT did not show any significant relationship with plasma lipoprotein levels. When subgroups of women with comparable ages and adiposity but with high and low intra-abdominal fat accumulation were compared, women with a high accumulation of intra-abdominal fat displayed significantly lower HDL-CHOL (p less than 0.001), HDL2-CHOL (p less than 0.001), HDL3-CHOL (p less than 0.01), and HDL-apo A-I (p less than 0.05) levels, as well as reduced HDL-CHOL/LDL-CHOL (p less than 0.01), HDL-apo A-I/LDL-apo B (p less than 0.05), and HDL2-CHOL/HDL3-CHOL ratios (p less than 0.05) in comparison with obese women with low accumulations of intra-abdominal fat.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗