Transforming Growth Factor-alpha Delays Gastric Emptying and Small Intestinal Transit in Suckling Rats

Abstract

Transforming growth factor-alpha (TGF-alpha) is a biologically potent polypeptide detected in the gastrointestinal tract in suckling rats. The major goal of the present study was to test the hypothesis that the administration of TGF-alpha affects gastric emptying and small intestinal transit in suckling rats. Suckling (12-day-old) rats fasted 16 h received rat TGF-alpha subcutaneously (s.c.) or orogastrically in varying doses (0, 0.5, 1.0 microg/rat in 0.1% BSA). Control animals received 0.1% BSA only. Poly R-478 dye was used as a motility marker. Rats were decapitated 45 min after marker administration and the amount of dye in the stomach and the small intestine was measured by spectrophotometry. Subcutaneous administration of TGF-alpha significantly delayed stomach evacuation. In controls, the stomach contained 21.4 +/- 1.4% (mean +/- s(x)) of the Poly R-478 marker, whereas in TGF-alpha treated rats the stomach contained 37.2 +/- 2.8% of the total Poly R-478 dye given to animals. The delaying effect of TGF-alpha was time- and dose-dependent. Small intestinal transit was also significantly delayed. The proximal jejunum of TGF-alpha treated rats contained a 1.4-fold higher amount of marker in comparison with control rats. Orogastrically administered rTGF-alpha did not affect gastric emptying or intestinal transit. In conclusion, s.c. administration of rat TGF-alpha significantly delayed the gastrointestinal motility in vivo in suckling rats.

EGFR is involved in control of gastric cell proliferation through activation of MAPK and Src signalling pathways in early-weaned rats

“…EGF and TGFα bind to the same receptor and have similar biological activity, but despite the presence of both peptides in the gastrointestinal tract, TGFα is more widely distributed and may be the main ligand for EGFR in this mucosa (19). TGFα is a multifunctional peptide, which stimulates cell proliferation, differentiation and migration (20–22), inhibits apoptosis (23), delays gastric emptying (24), inhibits acid secretion (25,26) and accelerates repair of lesions (27,28). In the gastric mucosa, TGFα and EGFR are detected in surface mucous, mucous neck and parietal cells (7,29,30).…”

Group A Rotavirus Infection and Age-Dependent Diarrheal Disease in Rats: a New Animal Model To Study the Pathophysiology of Rotavirus Infection

“…Gastrointestinal transit time in adult rats is Ͻ8 h and is approximately 16 h in suckling rats (30,36,63,65). As determined previously (7, 9), detection of virus shedding by ELISA and detection of infectious virus by FFA correlated (P Ͻ 0.001 and r ϭ 0.792; Pearson's correlation coefficient).…”

Effects of Bovine α-Lactalbumin on Gastric Defense Mechanisms in Naive Rats

“…33) Delay of gastric emptying [19][20][21]34) and inhibition of gastric contraction 22,23) have been shown to contribute to gastroprotection. Hypercontraction, an increase in gastric contraction, is a major pathogenic mechanism of ulcers induced by necrotizing agents 22) and stress.…”

“…[11][12][13] In addition to activation of PG synthesis, defense mechanisms of the gastric mucosa include stimulation of mucus 11,14) and bicarbonate secretion, 11,15,16) increase in gastric ‰uid volume, 17,18) and inhibition of gastric motility (emptying and contraction). [19][20][21][22][23][24] Under the hypothesis that a-LA aŠects these defense mechanisms, and strengthens gastric mucosa before exposure to damaging factors, we investigated the eŠects of a-LA on PGE2 content in gastric tissue, gastric mucin content, gastric luminal pH, gastric ‰uid volume, and gastric emptying in naive rats. We also examined the correlation between PG synthesis and the eŠects of a-LA on these defense mechanisms.…”