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

J Appl Physiol (1985). 1999 Aug;87(2):722-31. doi: 10.1152/jappl.1999.87.2.722.


Glucose utilization increases markedly in the normal dog during stress induced by the intracerebroventricular (ICV) injection of carbachol. To determine the extent to which insulin, glucagon, and selective (alpha/beta)-adrenergic activation mediate the increment in glucose metabolic clearance rate (MCR) and glucose production (R(a)), we used five groups of normal mongrel dogs: 1) pancreatic clamp (PC; n = 7) with peripheral somatostatin (0.8 microg x kg(-1) x min(-1)) and intraportal replacement of insulin (1,482 +/- 84 pmol x kg(-1) x min(-1)) and glucagon (0.65 ng x kg(-1) x min(-1)) infusions; 2) PC plus combined alpha (phentolamine)- and beta (propranolol)-blockade (7 and 5 microg x kg(-1) x min(-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 ICV carbachol stress (0-120 min), catecholamines, ACTH, and cortisol increased in all groups. Baseline insulin and glucagon levels were maintained in all groups except Con, where glucagon rose 33%, and alpha, where insulin increased slightly 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 was 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. Stress-induced lipolysis was abolished in beta (P < 0.05). The marked rise in lactate in Con, PC, and alpha was abolished in alpha+beta and beta. We conclude that the stress-induced increase in MCR is largely independent of changes in insulin, markedly augmented by beta-blockade, and related, at least in part, to inhibition of lipolysis and glycogenolysis, and that R(a) is augmented by glucagon and alpha- and beta-catecholamine effects.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenergic Agents / pharmacology
  • Animals
  • Blood Glucose / metabolism
  • Carbachol
  • Catecholamines / blood
  • Cerebral Ventricles
  • Dogs
  • Fatty Acids / blood
  • Glucagon / blood
  • Glucose / metabolism*
  • Hemodynamics / drug effects
  • Insulin / metabolism*
  • Lactic Acid / blood
  • Ligation
  • Male
  • Metabolic Clearance Rate
  • Pancreas / metabolism
  • Phentolamine / pharmacology
  • Stress, Physiological / chemically induced
  • Stress, Physiological / metabolism*


  • Adrenergic Agents
  • Blood Glucose
  • Catecholamines
  • Fatty Acids
  • Insulin
  • Lactic Acid
  • Carbachol
  • Glucagon
  • Glucose
  • Phentolamine