Role of endogenous somatostatin in postprandial hypersecretion of neurotensin in patients after gastrectomy.
prospective_cohort · Level II
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- Record sourced from PubMed, PMID 9114796.
- Also identified by PMC identifier 1190745.
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Abstract
The purpose of this report is to elucidate the mechanism of the hypersecretion of neurotensin (NT) after gastrectomy. NT secretion induced by fat ingestion is increased after pancreatoduodenectomy or distal gastrectomy. The hypersecretion of NT in the patients undergoing resection of the upper gastrointestinal tract is suppressed by an exogenous somatostatin (SST) analog. We observed simultaneously the secretion of NT and SST in the same patients before and after gastrectomy (n = 7). We also observed the secretion of these hormones induced by intraduodenal (ID) fat infusion in the normal volunteers (n = 6). The response of plasma NT to fat ingestion was significantly increased after gastrectomy compared with that before gastrectomy. The response of plasma SST after gastrectomy was significantly suppressed. The response of plasma NT and SST after ID fat infusion in the normal volunteers was similar to the gastrectomized state. Diminution of SST secretion, probably caused by the lack of SST cells in the distal part of the stomach, may play a role in augmenting NT secretion after gastrectomy.
Medical subject headings
- Gastrectomy
- Neurotensin
- Somatostatin