The diffuse neuroendocrine system in gastroenterology.

stimulating insulin release when taken orally (Marks & Samols, 1969), suggesting that its insulin-stimulating effect is mediated through one or more of the intestinal insulin-stimulating hormones. The degree of hyperglycaemia after ingestion of fructose or galactose is similar and small; however, ingestion of galactose elevates circulating concentrations of gastric inhibitory polypeptide, whereas fructose does not (Sykes et al., 1979). The stimulation of insulin secretion by galactose, but not fructose, is consistent with a gastric-inhibitory-polypeptide-mediated effect; when fructose is given, a similar degree of hyperglycaemia in the absence of elevated gastric-inhibitory-polypeptide concentrations is incapable of stimulating insulin secretion. Release of gastric inhibitory polypeptide is dependent on absorption of nutrient. Addition of phloridzin to an oral glucose load will inhibit both absorption of glucose and release of the polypeptide (Ebert & Creutzfeldt, 1978; Sykes et al., 1980), providing another mechanism to prevent inappropriate insulin secretion. Insulin can suppress release of gastric inhibitory polypeptide, providing a feedback-control mechanism, although the evidence as to whether insulin has the ability to inhibit both fat and glucose-induced polypeptide, or fat-induced polypeptide alone, is conflicting (Sirinek et al., 1978; Andersen et al., 1978). It is possible that an overactive entero-insular axis is involved in the pathogenesis of hyperinsulinaemia of obesity. Obese subjects have an exaggerated gastric-inhibitory-polypeptide response to fat and a mixed meal and the feedback control of the fat-induced polypeptide is also defective (Creutzfeldt el al., 1978).