Adrenergic blockade prevents endotoxin-induced increases in glucose metabolism

D. M. Hargrove, G. J. Bagby, C. H. Lang, J. J. Spitzer

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Abstract

Combined α- and β-adrenergic blockade was used to investigate the role of catecholamines in endotoxin-induced elevations in glucose kinetics. Glucose kinetics were measured before and for 4 h after the injection of endotoxin [100 μg/100 g body wt iv, 30% lethal dose (LD30) at 24 h]. Adrenergic blockade was achieved by the bolus injection of phentolamine and propranolol followed by their continuous infusion. Endotoxin-treated rats exhibited a transient hyperglycemia and sustained (>4 h) increase in plasma lactate concentration, as well as elevated rates of glucose appearance (R(a), 83%), disappearance (R(d), 58%), recycling (160%), and metabolic clearance (23%). Adrenergic blockade prevented endotoxin-induced increases in plasma glucose concentration, R(a), R(d), and recycling but not glucose clearance. The increase in plasma lactate concentration was blunted by 35%. After 2 h, endotoxic animals infused with adrenergic antagonists developed hypoglycemia, which may have resulted from an increased plasma insulin concentration. The attenuation of elevated glucose turnover by adrenergic blockade in the endotoxin-treated animals was not due to a reduction in plasma glucagon level or differences in plasma insulin concentration. Administration of the α- or β-adrenergic antagonists separately blunted but did not prevent endotoxin-induced changes in glucose kinetics, and therefore the efficacy of the adrenergic blockade could not be assigned to a single receptor class. These results indicate that catecholamines are important contributory factors to many of the early alterations in carbohydrate metabolism observed during endotoxemia.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume255
Issue number5
StatePublished - Dec 1 1988

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Endotoxins
Adrenergic Agents
Glucose
Adrenergic Antagonists
Recycling
Catecholamines
Lactic Acid
Insulin
Injections
Endotoxemia
Phentolamine
Carbohydrate Metabolism
Glucagon
Hypoglycemia
Propranolol
Hyperglycemia

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)

Cite this

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abstract = "Combined α- and β-adrenergic blockade was used to investigate the role of catecholamines in endotoxin-induced elevations in glucose kinetics. Glucose kinetics were measured before and for 4 h after the injection of endotoxin [100 μg/100 g body wt iv, 30{\%} lethal dose (LD30) at 24 h]. Adrenergic blockade was achieved by the bolus injection of phentolamine and propranolol followed by their continuous infusion. Endotoxin-treated rats exhibited a transient hyperglycemia and sustained (>4 h) increase in plasma lactate concentration, as well as elevated rates of glucose appearance (R(a), 83{\%}), disappearance (R(d), 58{\%}), recycling (160{\%}), and metabolic clearance (23{\%}). Adrenergic blockade prevented endotoxin-induced increases in plasma glucose concentration, R(a), R(d), and recycling but not glucose clearance. The increase in plasma lactate concentration was blunted by 35{\%}. After 2 h, endotoxic animals infused with adrenergic antagonists developed hypoglycemia, which may have resulted from an increased plasma insulin concentration. The attenuation of elevated glucose turnover by adrenergic blockade in the endotoxin-treated animals was not due to a reduction in plasma glucagon level or differences in plasma insulin concentration. Administration of the α- or β-adrenergic antagonists separately blunted but did not prevent endotoxin-induced changes in glucose kinetics, and therefore the efficacy of the adrenergic blockade could not be assigned to a single receptor class. These results indicate that catecholamines are important contributory factors to many of the early alterations in carbohydrate metabolism observed during endotoxemia.",
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Adrenergic blockade prevents endotoxin-induced increases in glucose metabolism. / Hargrove, D. M.; Bagby, G. J.; Lang, C. H.; Spitzer, J. J.

In: American Journal of Physiology - Endocrinology and Metabolism, Vol. 255, No. 5, 01.12.1988.

Research output: Contribution to journalArticle

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