Metabolic, hormonal, and hemodynamic changes induced by metabotropic excitatory amino acid agonist (1S,3R)-ACPD.
Metabolic, hormonal, and hemodynamic changes induced by metabotropic excitatory amino acid agonist (1S,3R)-ACPD.
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代谢型兴奋性氨基酸激动剂 (1S,3R)-ACPD 引起的代谢、激素和血流动力学变化。
DOI:
10.1152/ajpregu.1995.268.4.r1026
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发表时间:
1995
期刊:
影响因子:
--
通讯作者:
Ajmal,M
中科院分区:
文献类型:
--
作者:
Lang,CH;Ajmal,M
The purpose of the present study was to determine whether central administration of (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD), a selective metabotropic glutamate receptor agonist, would stimulate glucose metabolism, activate the hypothalamic-pituitary-adrenal axis, or influence pancreatic endocrine secretion. Intracerebroventricular injection of ACPD increased arterial glucose levels by 60% within 15 min, which were sustained throughout the 3-h experimental protocol. This hyperglycemia resulted from an early increase in hepatic glucose production (HGP, 88%) that exceeded the increase in glucose uptake by peripheral tissues (66%). Stimulation of glucose metabolism was associated with transient elevations in plasma insulin (145%) and glucagon (3-fold) levels and more sustained elevations in corticosterone (141%), epinephrine (3- to 5-fold), and norepinephrine (32-110%). Intravenous infusion of alpha- and beta-adrenergic antagonists prevented the ACPD-induced increase in glucose metabolism. Arterial blood pressure, cardiac index, and total peripheral resistance were not altered after ACPD. Overall, the changes in regional blood flow were unremarkable, although ACPD did increase blood flow to the liver (2-fold) and heart (48%) and decrease flow to the stomach (33%). These results indicate that central administration of ACPD 1) enhances HGP, which is primarily mediated by adrenergic stimulation; 2) increases glucose uptake by peripheral tissues, which appears to be mediated by both hyperinsulinemia and hyperglycemia; 3) stimulates pancreatic and adrenal hormone secretion independent of adrenergic activation; and 4) produces minimal changes in regional blood flow that cannot explain the glucose metabolic response produced by ACPD.(ABSTRACT TRUNCATED AT 250 WORDS)