The role of endogenous gastric inhibitory polypeptide in the enteroinsular axis.
In order to elucidate the relationship between the release of gastric inhibitory polypeptide ( GIP) and insulin, we compared plasma GIP and insulin concentration responses to meal ingestion in normal subjects and patients with various surgical modifications of the food pathway. Nine patients with Billroth I partial gastrectomy (BI), 7 patients with Billroth II partial gastrectomy ( BII), and 6 patients with total gastrectomy (TG) were tested. In BI patients the increase in blood glucose was similar to that in normal subjects, but the response was significantly greater in BII and TG patients. In TG patients blood glucose rose significantly higher in response to a standard meal than in all other groups. In BI patients the mean peak GIP level after meal ingestion was significantly higher than in normal subjects. In BII and TG patients an extremely exaggerated GIP response after the meal was observed. The insulin response to feeding was increased only in the BII and TG patients. Since the insulin response was enhanced only when both the glucose and GIP responses were magnified, we conclude that endogenous GIP is a glucose-dependent insulinotropic factor. In addition, from the fact that meal-stimulated GIP release is most marked in patients with total gastrectomy, we conclude that the direct contact of food with the GIP-producing cells is a strong mechanical or chemical stimulus for GIP release.[1]References
- The role of endogenous gastric inhibitory polypeptide in the enteroinsular axis. Takemura, J., Seino, Y., Yamamura, T., Tsuda, K., Seino, S., Itoh, N., Imura, H. J. Clin. Endocrinol. Metab. (1982) [Pubmed]
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