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PubMed1993

Effect of D-glucose on intestinal permeability and its passive absorption in human small intestine in vivo.

BACKGROUND: Based on studies in animals, it has been proposed that carrier-mediated D-glucose absorption markedly enhances passive permeability of the jejunal mucosa, allowing the majority of D-glucose absorption to proceed passively. In this study, we evaluated this hypothesis in the human jejunum in vivo. METHODS: Using the constant perfusion, nonabsorbable marker technique, permeability of jejunal mucosa was assessed by measuring the ratio of diffusion rates of urea/L-xylose and mannitol/L-xylose. Passive D-glucose absorption was quantitated using L-glucose and mannitol as probes for D-glucose. RESULTS: Addition of D-glucose to perfused solutions did not change the diffusion ratios, indicating that D-glucose has no effect on the size of channels for passive diffusion across the jejunal mucosa. The fraction of total D-glucose absorption that could be attributed to a passive mechanism averaged 5%. In the human ileum in vivo, we detected no evidence of passive D-glucose absorption. CONCLUSIONS: Carrier-mediated D-glucose absorption does not increase passive permeability of human jejunal mucosa to solutes with molecular radii between 2.6 and 4.0 A. The amount of D-glucose absorbed passively from the human jejunum is trivial compared with the overwhelmingly dominant mechanism, carrier-mediated transport. Our results do not support the concept that sodium-dependent nutrient transport increases tight junction permeability.

Glucose↗
PubMed1985

Mechanism of action of cholecystokinin on intestinal blood flow; interactions with opioid peptides and vasoactive intestinal peptide.

The effects of local administration of CCK-OP on mesenteric blood flow was studied in anaesthetized dogs using an electromagnetic flowmeter and interactions with the opioid peptides and VIP examined. CCK-OP was found to enhance enteral blood flow and tissue metabolism. Investigations with pharmacological antagonists showed that the vasoregulatory effect was exerted neurogenically, by influencing the activities of sympathetic alpha 2 adrenergic, dopaminergic, cholinergic, muscarinergic and nicotinic neurones. The flow-increasing action of CCK-OP was enhanced by D-Met2-NleS5-enkephalinamide; the effect was additive and partially blocked by naloxone. D-Met2-Pro5-enkephalinamide blocked the increases caused by CCK-OP in blood flow and tissue acetylcholine levels. The blockade was not competitive and could be totally eliminated by naloxone. VIP blocked the flow-increasing effect of CCK-OP by a non-competitive mechanism. The results provide data on the peptidergic regulatory mechanisms of the mesenteric circulation.

Acetylcholine↗