Increased gluconeogenesis in rats exposed to hyper-G stress

Abstract

The role of gluconeogenesis on the increase in plasma glucose and liver glycogen of rats exposed to hyper-G (radial acceleration) stress was determined. Overnight-fasted, male Sprague-Dawley rats (250–300 g) were injected i.p. with uniformly labeled 14C lactate, alanine, o rm glycerol (5μCi/rat) and immediately exposed to 3.1G for 0.25, 0.50, and 1.0 hr. 14C incorporation of the labeled substrates into plasma glucose and liver glycogen was measured and compared to noncetrifuged control rats injected in a similar manner. Significant increases in 14C incorporation of all three labeled substrates into plasma glucose were observed in centrifuged rats at all exposure periods; 14C incorporation into liver glycogen was significantly increased only at 0.50 and 1.0 hr. The i.p. administration (5 mg/100-g body wt) of 5-methoxyindole-2-carboxylic acid, a potent gluconeogenesis inhibitor, prior to centrifugation blocked the increase in plasma glucose and liver glycogen during the first hour of centrifugation. The increase in plasma glucose and liver glycogen was also abolished in adrenodemedullated rats exposed to centrifugation for 1.0 hr. Propranolol, a beta-adrenergic blocker, suppressed the increase in plasma glucose of rats exposed to centrifugation for 0.25 hr. From the results of this study, it is concluded that the initial, rapid rise in plasma glucose as well as the increase in liver glycogen of rats exposed to hyper-G stress can be attributed to an increased rate of gluconeogenesis, and that epinephrine plays a dominant role during the early stages of exposure to centrifugation.