BACKGROUND & AIMS: Insulin exerts a strict short-term control of glucose disappearance by glucose storage as well as degradation in the liver and peripheral insulin target tissues, but an acute control of glucose appearance by glucose absorption in the intestine is as yet unknown. The aim of the present study was to evaluate, whether insulin acutely modulates intestinal glucose absorption. METHODS: In the isolated, nonrecirculating joint perfusion of the small bowel and liver of the rat via the celiac trunc and the superior mesenteric artery, glucose absorption was examined without and with infusion of insulin via the portal vein. RESULTS: Portal insulin enhanced acutely intestinal glucose absorption. This thus far unknown stimulatory effect of portal insulin was dose-dependent and detectable at physiological insulin concentrations. Atropine infused into the superior mesenteric artery completely prevented the insulin-dependent increase in intestinal glucose absorption, and carbachol caused a similar increase as portal insulin. CONCLUSIONS: Portal insulin dose-dependently generated a signal in the liver or portal vein. This signal was transmitted in a retrograde direction against the blood stream in the portal vein to the small intestine via hepatoenteral muscarinic nerves. This signal markedly increased intestinal glucose absorption.
BACKGROUND & AIMS: Insulin exerts a strict short-term control of glucose disappearance by glucose storage as well as degradation in the liver and peripheral insulin target tissues, but an acute control of glucose appearance by glucose absorption in the intestine is as yet unknown. The aim of the present study was to evaluate, whether insulin acutely modulates intestinal glucose absorption. METHODS: In the isolated, nonrecirculating joint perfusion of the small bowel and liver of the rat via the celiac trunc and the superior mesenteric artery, glucose absorption was examined without and with infusion of insulin via the portal vein. RESULTS: Portal insulin enhanced acutely intestinal glucose absorption. This thus far unknown stimulatory effect of portal insulin was dose-dependent and detectable at physiological insulin concentrations. Atropine infused into the superior mesenteric artery completely prevented the insulin-dependent increase in intestinal glucose absorption, and carbachol caused a similar increase as portal insulin. CONCLUSIONS: Portal insulin dose-dependently generated a signal in the liver or portal vein. This signal was transmitted in a retrograde direction against the blood stream in the portal vein to the small intestine via hepatoenteral muscarinic nerves. This signal markedly increased intestinal glucose absorption.