Insulin-like growth factor I accelerates gastric ulcer healing by stimulating cell proliferation and by inhibiting gastric acid secretion

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 hy pothesized that IGF-I participates in the healing of gastric ulcers. The ai m of the study was to determine: 1) whether IGF-I applied locally would sup port gastric ulcer healing by increasing cell proliferation and 2) the effe ct 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 mug) or v ehicle was infiltrated perifocally. In another group, animals received a da ily dose of 40 mu mol omeprazole subcutaneously. Ulcer healing was evaluate d by ulcer size and histological examination at 7 days. Pentagastrin-stimul ated gastric acid secretion was evaluated in conscious rats with gastric fi stula, after IGF-1(400 mug) had been injected intravenously. Results: IGF-I significantly reduced ulcer size, but only at low doses (0.4 mug/kg body w eight (BW), P = 0.008; 4 mug/kg BW, P = 0.001). This effect was similar to omeprazole treatment. Histological examination after IGF-I administration s howed increased cell proliferation, increased IGF-I content and down-regula ted IGF-I receptors. The secretory studies demonstrated a significant decre ase in gastric acid secretion 30 min after IGF-I bolus injection (IGF-I: 53 +/- 11 mu Eq; vehicle: 116 +/- 5 mu Eq; P = 0.001), which lasted for more than 1 h. Conclusion: IGF-I stimulates gastric ulcer healing, stimulating c ell proliferation and inhibiting gastric acid secretion.