TY - JOUR
T1 - Glucose uptake during centrally induced stress is insulin independent and enhanced by adrenergic blockade
AU - Lekas, Michael C.
AU - Fisher, Simon J.
AU - El-Bahrani, Ban
AU - Van Delangeryt, Mayliza
AU - Vranic, Mladen
AU - Shi, Z. Qing
PY - 1999
Y1 - 1999
N2 - 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 (α/β)- 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 μg · kg-1 · min-1) and intraportal replacement of insulin (1,482 ± 84 pmol · kg-1 · min-1) and glucagon (0.65 ng · kg-1 · min-1) infusions; 2) PC plus combined α (phentolamine)- and β (propranolol)- blockade (7 and 5 μg · kg-1 · min-1, respectively; α+β; n = 5); 3) PC plus α-blockade (α; n = 6); 4) PC plus β-blockade (β; 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 α, where insulin increased slightly but significantly. Stress increased (P < 0.05) plasma glucose in Con, PC, and but decreased it in β and α+β. The MCR increment was greater (P < 0.05) in β and α+β than in Con, PC, and α. R(a) increased (P < 0.05) in all groups but was attenuated in α+β. Stress-induced lipolysis was abolished in β (P < 0.05). The marked rise in lactate in Con, PC, and α was abolished in α+β and β. We conclude that the stress-induced increase in MCR is largely independent of changes in insulin, markedly augmented by β-blockade, and related, at least in part, to inhibition of lipolysis and glycogenolysis, and that R(a) is augmented by glucagon and α- and β-catecholamine effects.
AB - 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 (α/β)- 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 μg · kg-1 · min-1) and intraportal replacement of insulin (1,482 ± 84 pmol · kg-1 · min-1) and glucagon (0.65 ng · kg-1 · min-1) infusions; 2) PC plus combined α (phentolamine)- and β (propranolol)- blockade (7 and 5 μg · kg-1 · min-1, respectively; α+β; n = 5); 3) PC plus α-blockade (α; n = 6); 4) PC plus β-blockade (β; 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 α, where insulin increased slightly but significantly. Stress increased (P < 0.05) plasma glucose in Con, PC, and but decreased it in β and α+β. The MCR increment was greater (P < 0.05) in β and α+β than in Con, PC, and α. R(a) increased (P < 0.05) in all groups but was attenuated in α+β. Stress-induced lipolysis was abolished in β (P < 0.05). The marked rise in lactate in Con, PC, and α was abolished in α+β and β. We conclude that the stress-induced increase in MCR is largely independent of changes in insulin, markedly augmented by β-blockade, and related, at least in part, to inhibition of lipolysis and glycogenolysis, and that R(a) is augmented by glucagon and α- and β-catecholamine effects.
KW - Glucose clearance
KW - Glucose production
KW - Pancreatic clamp
KW - Stress
KW - α-adrenergic blockade
KW - β-adrenergic blockade
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U2 - 10.1152/jappl.1999.87.2.722
DO - 10.1152/jappl.1999.87.2.722
M3 - Article
C2 - 10444633
AN - SCOPUS:0032817318
SN - 8750-7587
VL - 87
SP - 722
EP - 731
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
IS - 2
ER -