Reduction by morphine of human prosprandial insulin release is secondary to inhibition of gastrointestinal motility

The effect of morphine (0.1 mg/kg) on insulin secretion stimulated by oral, intraduodenal, or intravenous administration of glucose was studied in seven healthy volunteers. When glucose was given intravenously, morphine had no effect on plasma glucose, insulin, glucose-dependent insulinotropic polypeptide (GIP), or pancreatic glucagon. Following oral glucose, morphine slowed gastric emptying and reduced plasma concentrations of glucose, insulin, and GIP. During intraduodenal infusion of glucose, insulin concentrations of plasma were also decreased by morphine, an effect best explained by decreased small intestinal transit with delayed absorption of glucose and delayed release of GIP. We conclude that clinically relevant doses of morphine have no direct effect on insulin secretion and that the changes observed were secondary to slowed gastric emptying and small intestinal transit (AU)

Sugar absorption and intestinal motility in children when malnourished and after treatment

The ability of malnourished children to absorb lactose, sucrose and glucose was tested by perfusing the jejunum. Intestinal motility was measured simultaneously in a perfused segment by a dye dilution technique. These tests were repeated on the same children after 6-16 weeks of treatment. There was a significant correlation between the rate of hydrolysis of disaccharide perfusing the jejunum and the level of disaccharidase activity within the jejunal mucosa. All ten malnourished children had dimished glucose absorption, eight had reduced lactose and six had impaired sucrose hydrolysis and absorption. Children with the most severe mucosal damage had the lowest rate of sugar absorption. The malabsorption of disaccharide was related to the impairment of hydrolysis and not to the malabsorption of the monosaccharide products. Primary hypermotility of the intestine was not a feature of the malnourished group. Water absorption from all infusions occurred only in the treated group. Water entry into the intestinal lumen in the malnourished group was greatest with the most poorly absorbed sugars. The mean transit time of fluid passing down the intestine was inversely correlated with the sugar remaining unabsorbed within the lumen. Treating the malnourished child in hospital produced an increase in glucose, lactose and sucrose absorption. The generalized nature of the malabsorption and the reversibility of the defects suggests that lactose intolerance in these children is related to the nutritional state and not to a genetic predisposition to lactase deficiency. (Summary)