Glucose uptake during centrally induced stress is insulin independent and enhanced by adrenergic blockade

Glucose utilization increases markedly in the normal dog during stress indu ced by the intracerebroventricular (ICV) injection of carbachol. To determi ne the? extent to which insulin, glucagon, and selective (alpha/beta)-adren ergic activation mediate the increment in glucose metabolic clearance rate (MCR) and glucose production (R-a), we used five groups of normal mongrel d ogs: 1) pancreatic clamp (PC; n =7)with peripheral somatostatin (0.8 mu g . kg(-1) . min(-1)) and intraportal replacement of insulin (1,482 +/- 84 pmo l . kg(-1) . min(-1)) and glucagon (0.65 ng . kg(-1) . min(-1)) infusions; 2) PC plus combined alpha (phentolamine)- and beta (propranolol)-blockade ( 7 and 5 mu g . kg(-1) . m(-1), respectively; alpha+beta; n = 5); 3) PC plus alpha-blockade (alpha; n = 6); 4) PC plus beta-blockade (beta; n = 5); and 5) a carbachol control group without PC (Con, n = 10). During ICN carbacho l stress (0-120 min), catecholamines, ACTH, and cortisol increased in all g roups. Baseline insulin and glucagon levels were maintained in all groups e xcept Con, where glucagon rose 33%, and alpha, where insulin increased slig htly but; significantly. Stress increased (P < 0.05) plasma glucose in Con, PC, and alpha but decreased it in beta and alpha+beta. The MCR increment w as greater (P < 0.05) in beta and alpha+beta than in Con, PC, and alpha. R- a increased (P < 0.05) in all groups but was attenuated in alpha+beta Stres s-induced lipolysis was abolished in beta (P < 0.05). The marked rise in la ctate in Con, PC, and or was abolished in alpha+beta and beta. We conclude that the stress-induced increase in MCR is largely independent of changes i n insulin, markedly augmented by beta-blockade, and related, at least in pa rt, to inhibition of Lipolysis and glycogenolysis,and that R-a is augmented by glucagon and alpha- and beta-catecholamine effects.