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

Abstract

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 < .01) and ADM (12.4 ± 1.7 v 21.1 ± 1.2 mmol/L; P < .01) groups, with values lower in ADM-DT than in SHAM-DT rats ( P < .05). After glucose loading, the glucose levels were significantly lower ( P < .01) throughout the test in both SHAM-DT and ADM-DT rats than in their sedentary counterparts. The glucose levels were significantly lower ( P < .05) in ADM-DT than in SHAM-DT during the first 15 minutes following the glucose load, but the increase in glucose above baseline was not different between the two trained groups ( P = .1234). Physical training was associated with a twofold increase in basal plasma insulin levels in SHAM-DT (142 ± 22 v 53 ± 8 pmol/L; P < .01) and ADM-DT (201 ± 38 v 79 ± 19 pmol/L; P < .01) rats, compared with their sedentary counterparts. After glucose loading, a significant increase in plasma insulin levels was observed in the two trained diabetic groups, with greater values in ADM-DT than in SHAM-DT during the first 6 minutes, but the peak response in insulin was not different between both groups of trained animals ( P = .1386). In the two sedentary diabetic groups, the insulin levels were not significantly altered by the glucose load. Plasma glucagon levels in the basal state were not different between each of the four diabetic groups and the normal group. Although the glucose load induced a rapid decrease in glucagon levels in control rats, in diabetic animals this decrease was significantly delayed by 15 minutes in both sedentary groups, by 10 minutes in SHAM-DT, and by 6 minutes in ADM-DT animals. Thereafter, plasma glucagon levels returned progressively to basal values in each group of rats. Pancreatic insulin content was greatly diminished in all diabetic groups. Although pancreatic insulin content was not affected by adrenodemedullation, it was significantly greater in both SHAM (12.8 ± 2.9 v 3.8 ± 0.7 μg; P < .05) and ADM trained rats (19.4 ± 4.5 v 3.1 ± 0.7 μg; P < .01) than in their sedentary counterparts. Pancreatic glucagon content was increased in each diabetic group, but was not further modified by training or adrenodemedullation. These results indicate that adrenodemedullation, per se, had no effect on glucose homeostasis and insulin secretion in sedentary diabetic rats. However, physical training induced an improvement in the diabetic state, which seemed to be further increased in ADM rats, but this was probably due to a somewhat less severely diabetic state at the beginning.