Vagal glucose receptors, or glucose-sensitive units which modulate insulin secretion, exist in the liver. This study sought to determine the pathway of portal glucose-sensitive unit-regulated insulin secretion by measuring plasma insulin after intraperitoneal (IP) injection of glucose under unanesthetized and unrestrained conditions (Experiment 1), and by recording electrical discharge after intraportal injection of glucose (Experiment 2) in rats with hepatic and/or celiac vagotomy. In Experiment 1, plasma insulin was significantly reduced and plasma glucose elevated after IP glucose injection (1 g/kg) in the three groups of hepatic-, celiac-, and hepatic- and celiac-vagotomized rats in comparison with a sham-vagotomized group. There were no significant differences among the four groups in plasma insulin or glucose after IV glucose injection (0.5 g/kg). In Experiment 2, intraportal injection of 400 mg/dl of glucose solution, a similar concentration to that produced by 1 g/kg of IP glucose injection, caused a reduction in the discharge rate of hepatic vagal afferents and an increase in that of pancreatic vagal efferents. This increase was blocked by prior sectioning of the hepatic branch of the vagus nerve. These results suggested that hepatic glucose-sensitive units enhance glucose-induced insulin secretion via the hepatic vagal afferents and the pancreatic vagal efferents mediated by the brain stem center in vivo. The physiological role of these hepatic glucose-sensitive units is assumed to maintain blood glucose homeostasis by enhancing glucose-induced insulin secretion. © 1993.
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