Scandinavian journal of gastroenterology · 2001
Insulin-like growth factor I accelerates gastric ulcer healing by stimulating cell proliferation and by inhibiting gastric acid secretion.
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Coerper S, Wolf S, von Kiparski S, Thomas S, Zittel T T, Ranke M B, Hunt T K, Becker H D
Аннотация
BACKGROUND: Given the importance of Insulin-Like Growth Factor I (IGF-I) to intestinal maintenance and the presence of IGF-I in salivary glands, we hypothesized that IGF-I participates in the healing of gastric ulcers. The aim of the study was to determine: 1) whether IGF-I applied locally would support gastric ulcer healing by increasing cell proliferation and 2) the effect of IGF-I on gastric acid secretion.
METHODS: Gastric ulcers were induced with a cryoprobe. Immediately thereafter, IGF-I (0.4, 4.0 and 40 microg) or vehicle was infiltrated perifocally. In another group, animals received a daily dose of 40 micromol omeprazole subcutaneously. Ulcer healing was evaluated by ulcer size and histological examination at 7 days. Pentagastrin-stimulated gastric acid secretion was evaluated in conscious rats with gastric fistula, after IGF-I (400 microg) had been injected intravenously.
RESULTS: IGF-I significantly reduced ulcer size, but only at low doses (0.4 microg/kg body weight (BW), P = 0.008; 4 microg/kg BW, P = 0.001). This effect was similar to omeprazole treatment. Histological examination after IGF-I administration showed increased cell proliferation, increased IGF-I content and down-regulated IGF-I receptors. The secretory studies demonstrated a significant decrease in gastric acid secretion 30 min after IGF-I bolus injection (IGF-I: 53 +/- 11 microEq; vehicle: 116 +/- 5 microEq; P=0.001), which lasted for more than 1 h.
CONCLUSION: IGF-I stimulates gastric ulcer healing, stimulating cell proliferation and inhibiting gastric acid secretion.
METHODS: Gastric ulcers were induced with a cryoprobe. Immediately thereafter, IGF-I (0.4, 4.0 and 40 microg) or vehicle was infiltrated perifocally. In another group, animals received a daily dose of 40 micromol omeprazole subcutaneously. Ulcer healing was evaluated by ulcer size and histological examination at 7 days. Pentagastrin-stimulated gastric acid secretion was evaluated in conscious rats with gastric fistula, after IGF-I (400 microg) had been injected intravenously.
RESULTS: IGF-I significantly reduced ulcer size, but only at low doses (0.4 microg/kg body weight (BW), P = 0.008; 4 microg/kg BW, P = 0.001). This effect was similar to omeprazole treatment. Histological examination after IGF-I administration showed increased cell proliferation, increased IGF-I content and down-regulated IGF-I receptors. The secretory studies demonstrated a significant decrease in gastric acid secretion 30 min after IGF-I bolus injection (IGF-I: 53 +/- 11 microEq; vehicle: 116 +/- 5 microEq; P=0.001), which lasted for more than 1 h.
CONCLUSION: IGF-I stimulates gastric ulcer healing, stimulating cell proliferation and inhibiting gastric acid secretion.