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Effects of keratinocyte growth factor (KGF) on gut growth and repair
Author(s) -
Playford Raymond J.,
Marchbank Tania,
Mandir Nirmala,
Higham Andrew,
Meeran Karim,
Ghatei Mohammed A.,
Bloom Stephen R.,
Goodlad Robert A.
Publication year - 1998
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(199803)184:3<316::aid-path3>3.0.co;2-#
Subject(s) - keratinocyte growth factor , gastrointestinal tract , medicine , endocrinology , gastrin , small intestine , biology , growth factor , secretion , receptor
Keratinocyte growth factor (KGF) is a mitogen found throughout the gastrointestinal tract, but its role in gastrointestinal pathophysiology is unclear. The effect of recombinant KGF on gut growth and repair has been examined using a variety of in vivo models. Rats receiving total parenteral nutrition had co‐infusions of KGF or control for 6 days. Changes in gut growth (wet weight and vincristine‐induced metaphase arrest) were then assessed. The effects of KGF on gastric repair and acid secretion in rats were determined using an indomethacin (20 mg/kg)/restraint model and animals fitted with chronic gastric fistulae. KGF at 0·1, 1, and 3 mg/kg increased gut growth as assessed by wet weight throughout the gastrointestinal tract and increased vincristine‐induced accumulation of metaphases in the stomach and small intestine but not in the colon. Plasma gastrin, peptide YY, enteroglucagon, and glucagon‐like peptide‐1 were all increased, whereas insulin was lowered by KGF (all P <0·01). KGF was ineffective in reducing indomethacin‐induced gastric damage but caused a reduction in basal acid secretion of about 35 and 50 per cent when administered at 0·2 or 5 mg/kg ( P <0·05). These studies support the idea that KGF is involved in the control of proliferation of the gastrointestinal tract. They do not provide evidence, however, for a role in the early reparative process invoked during short‐term models of gastrointestinal injury. © 1998 John Wiley & Sons, Ltd.