Functional development of the stomach.
Large increases in gastric acid and pepsin secretion, antral gastrin concentration, and decreases in serum gastrin occur during the third week of life in the neonatal rat. At the same time gastrin receptors appear and gastrin release becomes sensitive to somatostatin, indicating that absence and then appearance of specific hormone receptors may be responsible for some of the ontogenic pattern. At this time the mucosa also begins to grow rapidly, with a greater proportion of cells leaving the proliferative pool and differentiating. For the first 2.5-3 weeks these ontogenic changes can be triggered by corticosterone. Their full expression depends on dietary changes associated with weaning. Neither hormones, dietary changes, nor the weaning process itself is essential for development, because in the absence of these, all of the changes still occur--although they may be delayed or be smaller in magnitude. Figure 1 provides a generalized summary of the normal functional development of the stomach and how it is altered by changes in corticosterone levels and the absence of weaning. These findings indicate that ontogeny is genetically programmed and that the full expression of this program depends on hormones, luminal contents, and other environmental factors. In comparison with the small intestine, for example, gastric ontogeny has not received adequate attention. There are essentially no studies directed toward understanding changes in motility during this period. There is really only one study examining the growth pattern of the mucosa during development, and this study is aimed at changes in DNA synthesis and cell loss. Experiments involving the cell cycle are needed to understand whether existing cells mature and differentiate or whether newly created cells suddenly leave the proliferative pool to differentiate. There have been no experiments in which the effects of thyroid hormone on gastric development have been adequately examined. In addition, little or nothing is known about EGF in the ontogenic process. Studies implanting fetal tissue into adult hosts are needed to determine which gastric functions can develop in the absence of luminal stimulation and hormone changes. The cell biology of the gastric mucosa is difficult to examine--especially that involving the cells concerned with growth and differentiation. The stem cells are dispersed throughout the tissue and are a small portion of the cell population. These have never been isolated for study. In vitro culture of mucosal cells, however, is a technique that can possibly be used to examine development at the cellular and molecular level.
D000818:Animals; D004032:Diet; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism*; D005755:Gastrins / Q000378:metabolism; D005768:Gastrointestinal Hormones / Q000378:metabolism*; D005769:Gastrointestinal Motility; D005938:Glucocorticoids / Q000502:physiology; D006632:Histamine / Q000494:pharmacology; D010434:Pepsin A / Q000378:metabolism; D010435:Pepsinogens / Q000378:metabolism; D051381:Rats; D013268:Stimulation, Chemical; D013270:Stomach / Q000254:growth & development / Q000502:physiology*; D013963:Thyroid Hormones / Q000502:physiology; D014886:Weaning
D005755:Gastrins; D005768:Gastrointestinal Hormones; D005938:Glucocorticoids; D010435:Pepsinogens; D013963:Thyroid Hormones; D006632:Histamine; D010434:Pepsin A