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Dietary protein stimulates pancreatic growth via CCK‐independent mTOR activation
Author(s) -
Crozier Stephen James,
Williams John A
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.984.5
Subject(s) - medicine , endocrinology , calcineurin , pi3k/akt/mtor pathway , cholecystokinin , mapk/erk pathway , chemistry , pancreas , biology , signal transduction , receptor , biochemistry , transplantation
Dietary protein can stimulate pancreatic growth in the absence of CCK release, but there is little data on the regulation of CCK‐independent growth. To identify mechanisms whereby protein stimulates pancreatic growth, male C57BL/6 and CCK‐null mice were fed control (20% protein) or protein‐enriched (75% protein) chow for 7 days. The weight of the pancreas increased by 32% in C57BL/6 mice and 36% in CCK‐null mice. Changes in pancreatic weight in C57BL/6 mice were due primarily to cell hypertrophy; with a 68% increase in protein content and a 24% increase in DNA content. Parallel changes were observed in CCK‐null mice. ERK, calcineurin, and mTOR are activated in models of CCK‐induced growth, but there were no differences in ERK or calcineurin activation between fasted and fed CCK‐null mice. In contrast, mTOR activation was increased after feeding and the duration of activation was prolonged in mice fed protein‐enriched chow compared to control chow. Changes in pancreatic weight and DNA content were completely inhibited, and changes in protein content were partially abated, when the mTOR inhibitor rapamycin was administered during protein‐enriched chow feeding. Thus, dietary protein stimulates pancreatic growth in the absence of CCK via prolonged mTOR activation.