Effect of endogenous intestinal glucagon-like immunoreactivity (GLI) on insulin secretion and glucose concentration in dogs

Glucagon-like immunoreactivity (GLI), which is released from the gut during glucose absorption, has been regarded as having insulin-stimulating and perhaps glycogenolytic activity. Because purified GLI, free of other gut hormones, is not available to permit direct testing of these possibilities, the effect of endogenous GLI on insulin release and glucose concentration was determined by stimulating its release with substances other than glucose, which do not themselves influence insulin secretion. To find such substances, 2 g/kg of various monosaccharides was administered intraduodenally to conscious dogs as a 5% solution. Galactose and 3-O-methyl glucose, which are actively absorbed via the glucose carrier, both caused a rise in GLI, exceeding 2 ng/ml; this was unassociated with a significant rise in insulin. Fructose, facilitatively absorbed via a fructose carrier, also induced a rise in GLI, averaging over 1 ng/ml, which was unassociated with a rise in insulin or glucose. Passively absorbed xylose and mannose similarly elicited a GLI rise averaging at its peak, respectively, 1.7 and 2.0 ng/ml above the baseline, but again neither insulin nor glucose rose. In summary, it has been shown that the release of GLI is induced in dogs by the absorption of galactose, 3-O-methyl glucose, fructose, xylose and mannose, and that the rise in GLI induced by these monosaccharides is unaccompanied by a rise in insulin, or, except in the case of 3-O-methyl glucose, a rise in glucose. It seems unlikely, therefore, that the quantities of GLI released during the absorption of these sugars has either insulin-stimulating or glycogenolytic activity.