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Enteroglucagon, but not CCK, plays an important role in pancreatic hyperplasia after proximal small bowel resection
Author(s) -
SASAKI MASAYA,
BAMBA TADAO,
HOSADA SHIRO
Publication year - 1994
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.1994.tb01564.x
Subject(s) - medicine , cholecystokinin , endocrinology , gastrin , hyperplasia , gastrointestinal hormone , pancreas , biology , peptide hormone , receptor , secretion
The present study was performed to examine the role played by pancreatotrophic factors, especially enteroglucagon and cholecystokinin (CCK), in the compensatory pancreatic hyperplasia observed after proximal small bowel resection (PSBR). Male Wistar rats were randomized into two groups, receiving either PSBR or transection (TRC). Five animals from each group were randomly selected for treatment with FK‐480, a novel CCK antagonist. Four weeks after the operation, plasma levels of gastrin, CCK and enteroglucagon were measured. Pancreatic wet weight and protein, DNA, RNA and enzyme content were also determined. The wet weight and content of protein, DNA and RNA were significantly higher in PSBR rats than in TRC rats, regardless of whether they received FK‐480. FK‐480 had no suppressive effects on adaptive pancreatic growth after PSBR. Plasma enteroglucagon levels rose significantly in PSBR rats, and there were positive correlations between plasma enteroglucagon levels and pancreatic protein, DNA and RNA content. These findings demonstrated that plasma CCK was not the major trophic factor operating in the pancreas after PSBR, and showed that enteroglucagon plays an important role in the pancreatic hyperplasia that occurs after PSBR.