Hyper-G stress-induced hyperglycemia in rats mediated by glucoregulatory hormones.

Fasted male Sprague-Dawley rats, weighing 250-300 g, were exposed to 3.1 G for 0.25-24 h. During the first 24 h, there was a significant and sustained increase in plasma glucose, insulin, and glucagon. Plasma catecholamines showed significant increases only at 0.25 and 0.50 h, returning to control levels between 1.0-24 h; blood lactate paralleled the catecholamines' response. Plasma free glycerol showed a significant and sustained decrease during the first 24 h. Liver glycogen was significantly increased at 0.50 h, with progressively larger amounts accumulated as the exposure time was extended to 24 h. Diaphragm muscle glycogen was significantly decreased at 1.0 h, but showed a significant increase at 24 h. The isolated diaphragm muscle tissues from these rats were also studied in vitro to determine insulin effect on glucose uptake. Muscle tissues obtained from noncentrifuged controls and incubated with insulin (0.3 mU X ml-1) in the medium showed significant increases in glucose uptake; in contrast, muscle tissues from centrifuged rats showed no insulin effect on glucose uptake. It is concluded that the initial, rapid rise in blood glucose of rats exposed to hyper-G stress is mediated by increases in circulating catecholamines and glucagon, both potent stimulators of hepatic gluconeogenesis; and that the sustained hyperglycemia may be due in part to the inhibition of the insulin-stimulated uptake by muscle tissues.