ドパミンD₂受容体による血糖調節に対する視床下部ならびに側坐核の関与

抄録

The central nervous system might regulate glucose homeostasis, but its mechanism is unclear. We investigated the role of central dopamine D₂ receptors in glucose homeostasis. I.c.v. injection of both dopamine D₂ receptor agonist quinpirole and antagonist l-sulpiride increased plasma glucose levels. Hyperglycemia induced by quinpirole or l-sulpiride was diminished following fasting which decreases hepatic glycogen level, and these drugs did not affect hyperglycemia in the pyruvate tolerance test. Injection of β₂ adrenoceptor antagonist ICI 118,551, which blocks input from the sympathetic nerves to the liver, inhibited hyperglycemia induced by l-sulpiride, but not quinpirole, whereas hyperglycemia induced by quinpirole, but not l-sulpiride, was inhibited by hepatic vagotomy which blocks input from parasympathetic nerves. In addition, injection of quinpirole into the hypothalamus or nucleus accumbens increased plasma glucose levels, which was blocked by l-sulpiride. Taken together, it is suggested that stimulation of central dopamine D₂ receptors including the hypothalamus and the nucleus accumbens causes hyperglycemia by increasing hepatic glycogenolysis through parasympathetic nerves whereas blockade of central dopamine D₂ receptors causes hyperglycemia by increasing hepatic glycogenolysis through parasympathetic nerves.