Effects of Human Milk Growth Factor on Gastric and Duodenal Mucus Formation
A polypeptide growth factor has been isolated from human milk, and designated human milk growth factor III (1–3). It is chemically related to epidermal growth factor-urogastrone, having a molecular weight of about 6,000 and an isoelectric point of about 4.5 (1–3). EGF-urogastrone is a potent mitogen for a variety of cells (4) and is known to stimulate the growth and maturation of the intestinal mucosa (5, 6). The detection and isolation of epidermal growth factor (EGF) in human milk have also been reported by several other laboratories (7,8,9,10). Besides being a mitogen, EGF-urogastrone is an inhibitor of gastric acid secretion (11) and has been used to promote healing of ulcers (12). Thus, it is conceivable that human milk grcwth factor III (HMGF III) may also have urogastrone-like effects on the gastrointestinal tract. In a previous study, we demonstrated that HMGF III was capable of dose-dependently protecting mice against the formation of duodenal ulcers induced by cysteamine (13). These results are in agreement with those reported by Kirkegaard et al (14) that EGF significantly inhibits the formation of cysteamine-induced duodenal ulcer in the rat. However, the mechanisms remain unclear. It has been reported that cysteamine causes a long-lasting hypersecretion of gastric acid (15) and inhibits secretion of alkaline mucus from duodenal Brunner’s glands (16). Therefore, it is possible that HMGF III could have exerted its anti-ulcer effects in mice by altering gastric acid and/or duodenal mucus synthesis in a pattern opposite to that evoked by cysteamine. In order to clarify the mechanisms of the anti-ulcer actions of HMGF III, the present study examines its effects on gastric acid secretion and mucus formation in the mouse stomach and duodenum.
KeywordsDuodenal Ulcer Human Milk Gastric Acid Secretion Intragastric Administration Atropine Sulfate
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