Submitted on October 2, 2006
Accepted on April 25, 2007
Mechanism of rapid-phase insulin response to elevation of portal glucose concentration
Makiko Fukaya1, Akira Mizuno2*, Hidekazu Arai3, Kazusa Muto3, Takashi Uebanso4, Kaoru Matsuo5, Hironori Yamamoto3, Yutaka Taketani3, Toshio Doi6, and Eiji Takeda3
1 Departments of Clinical Nutrition, University of Tokushima School of Medicine, tokushima, Japan
2 Departments of Clinical Biology and Medicine, University of Tokushima School of Medicine, Tokushima, Japan
3 Tokushima, Japan; Departments of Clinical Nutrition, University of Tokushima School of Medicine, tokushima, Japan
4 Departments of Clinical Nutrition, University of Tokushima School of Medicine, Tokushima, Japan
5 tokushima, Japan; Departments of Clinical Nutrition, University of Tokushima School of Medicine, tokushima, Japan
6 Departments of Clinical Biology and Medicine, University of Tokushima School of Medicine, Japan
* To whom correspondence should be addressed. E-mail: mizuno{at}clin.med.tokushima-u.ac.jp.
The hepatoportal region is important for glucose sensing, however, the relationship between the hepatoportal glucose sensing system and the postprandial rapid phase of the insulin response has been unclear. We examined whether a rapid-phase insulin response to low amounts of intraportal glucose infusion would occur, compared that to the response to intrajugular glucose infusion in conscious rats, and assessed whether this sensing system was associated with autonomic nerve activity. The increases in plasma glucose concentration did not differ between the two infusions at 3 min, but the rapid-phase insulin response was only detected in the intraportal infusion. A sharp and rapid insulin response was observed at 3 min after intraportal infusion of small amount of glucose but not after intrajugular infusion. Furthermore, this insulin response was also induced by intraportal fructose infusion but not by nonmetabolizable sugars. The rapid-phase insulin response at 3 min during intraportal infusion did not differ between rats that had undergone hepatic vagotomy (Hx) or chemical sympathectomy with 6-hydroxydopamine (6-OHDA) compared with control rats, but this response disappeared in rats that had undergone chemical vagotomy with atropine. We conclude that the elevation of glucose concentration in the hepatoportal region induced afferent signals from undetectable sensors and that these signals stimulate pancreas to induce the rapid-phase insulin response via cholinergic nerve action.
