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 language||English (US)|
|Journal||American Journal of Physiology - Endocrinology and Metabolism|
|Issue number||1 30-1|
|State||Published - 1994|
All Science Journal Classification (ASJC) codes
- Endocrinology, Diabetes and Metabolism
- Physiology (medical)