Contribution of central and peripheral adrenergic stimulation to IL-1α- mediated glucoregulation

F. Petit, A. Jarrous, R. D. Dickinson, P. E. Molina, N. N. Abumrad, C. H. Lang

Research output: Contribution to journalArticle

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Abstract

The present study determined the contribution of central adrenoceptors and the peripheral sympathetic nervous system in regulating the hormonal and glucose metabolic response to intracerebroventricular injection of interleukin (IL)-1α. After an overnight fast, hepatic glucose production (HGP) and peripheral glucose uptake (GU) were assessed in catheterized conscious unrestrained rats using [3-3H]glucose. Intracerebroventricular injection of IL-1α (100 ng) produced a hyperglycemia that resulted from an early increase in HGP (108%) that exceeded a smaller elevation (82%) in GU. Intracerebroventricular injection of the α- and β-adrenergic antagonists phentolamine and propranolol before IL-1α blunted the glucose metabolic response 30-50%. This attenuated response was associated with normalization of the IL-1α-induced hyperglucagonemia and hyperinsulinemia and a 50-60% reduction in the incremental increase in plasma catecholamines. In contrast to central administration, systemic infusion of adrenergic blockers completely prevented the IL-1α-induced increases in plasma glucose, as well as HGP and GU. In these rats, the elevated plasma levels of insulin, glucagon, and corticosterone produced by intracerebroventricular injection of IL-1α were still present. The results indicate that 1) the enhanced whole body glucose metabolism seen after central administration of IL-1α is mediated by increased sympathoadrenal activity and 2) the IL-1α-induced increase in pancreatic insulin and glucagon secretion as well as part of the peripheral catecholamine release is mediated by central adrenoreceptors.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume267
Issue number1 30-1
StatePublished - Jan 1 1994

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Interleukin-1
Adrenergic Agents
Glucose
Injections
Adrenergic Antagonists
Glucagon
Catecholamines
Liver
Insulin
Phentolamine
Sympathetic Nervous System
Peripheral Nervous System
Hyperinsulinism
Corticosterone
Propranolol
Hyperglycemia
Adrenergic Receptors

All Science Journal Classification (ASJC) codes

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

Cite this

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abstract = "The present study determined the contribution of central adrenoceptors and the peripheral sympathetic nervous system in regulating the hormonal and glucose metabolic response to intracerebroventricular injection of interleukin (IL)-1α. After an overnight fast, hepatic glucose production (HGP) and peripheral glucose uptake (GU) were assessed in catheterized conscious unrestrained rats using [3-3H]glucose. Intracerebroventricular injection of IL-1α (100 ng) produced a hyperglycemia that resulted from an early increase in HGP (108{\%}) that exceeded a smaller elevation (82{\%}) in GU. Intracerebroventricular injection of the α- and β-adrenergic antagonists phentolamine and propranolol before IL-1α blunted the glucose metabolic response 30-50{\%}. This attenuated response was associated with normalization of the IL-1α-induced hyperglucagonemia and hyperinsulinemia and a 50-60{\%} reduction in the incremental increase in plasma catecholamines. In contrast to central administration, systemic infusion of adrenergic blockers completely prevented the IL-1α-induced increases in plasma glucose, as well as HGP and GU. In these rats, the elevated plasma levels of insulin, glucagon, and corticosterone produced by intracerebroventricular injection of IL-1α were still present. The results indicate that 1) the enhanced whole body glucose metabolism seen after central administration of IL-1α is mediated by increased sympathoadrenal activity and 2) the IL-1α-induced increase in pancreatic insulin and glucagon secretion as well as part of the peripheral catecholamine release is mediated by central adrenoreceptors.",
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Contribution of central and peripheral adrenergic stimulation to IL-1α- mediated glucoregulation. / Petit, F.; Jarrous, A.; Dickinson, R. D.; Molina, P. E.; Abumrad, N. N.; Lang, C. H.

In: American Journal of Physiology - Endocrinology and Metabolism, Vol. 267, No. 1 30-1, 01.01.1994.

Research output: Contribution to journalArticle

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T1 - Contribution of central and peripheral adrenergic stimulation to IL-1α- mediated glucoregulation

AU - Petit, F.

AU - Jarrous, A.

AU - Dickinson, R. D.

AU - Molina, P. E.

AU - Abumrad, N. N.

AU - Lang, C. H.

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