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• W2066476087 abstract "Upper alimentary epithelium is the first body tissue to encounter the food we eat. Although digestion starts in the stomach, the absorption of nutrients is almost exclusively the function of the proximal small bowel, being normally completed within the jejunum [1]. The distal small bowel has specialised transport mechanisms for bile acids and vitamin B j,. Otherwise it may play little part in the normal absorption of food, though it does provide a functional reserve if the jejunum is diseased or resected and perhaps if a particularly rich meal is consumed [2,3]. Since the small intestine is less efficient at absorbing fat than protein or carbohydrate, steatorrhoea dominates the short bowel syndrome [4]. The structure of the various segments of the intestinal tract reflects their different functional roles. Surgeons can quickly differentiate between healthy proximal and distal small bowel, because jejunum has a greater calibre than ileum and its wall is thicker. On palpation the jejunal mucosa can be appreciated as a separate layer from the muscularis, like feeling a shirtsleeve through one's jacket. Experimental data confirm a progressive decrease in mucosal mass between pylorus and ileocaecat valve [2]. The presence of proiecting villi enormously increases the surface area of the small bowel and is presumably needed for adequate mucosal uptake of nutrients and minerals. The large bowel absorbs water and electrolytes but nutrients hardly at all; villi are clearly unnecessary for this simpler absorptive process. All body tissues atrophy during starvation, but the small bowel is especially at risk. Hypoplastic changes are detectable after 24-48 h of fasting [5]. By 6 days the mass of enteric mucosa is depleted by a half, while that of other organs has only diminished by a third [6]. As anticipated the jejunum, which is consistently exposed to high concentrations of nutrients in ordinary life, is more susceptible to starvation than the ileum, which is not used to this environment [3,7]. Surprisingly the large bowel is also very sensitive to withdrawal of food [8,9]. There is evidence to show that faecal bulk alone can maintain the integrity of colonic (but not enteric) mucosa [I0]. The hypoplastic changes seen in the gut during starvation are reproduced by surgical exclusion from the intestinal stream. Agaitl bypassed jejunum atrophies more rapidly than bypassed ileum [11,12]. It is notable that cell turnover continues even when the epithelium is profoundly atrophic [13]. Perhaps that is why regeneration occurs so promptly when bypassed bowel is replaced in circuit or feeding is resumed [2,9]. Intestinal defunction does not appear to cause any irreversible changes. Similar hypoplastic changes to those in the small bowel can be found in the distal colorectum of rats given a diverting proximal colostomy. The contents of protein, RNA and DNA are diminished by a third at one week and by a halfat 4 weeks [14]. Once the colostomy is closed, the 'lost' tissue is exactly recovered within one week. The mechanisms that regulate intestinal mass must clearly be very precise, especially for such a rapidly renewing tissue. There is some type of local feedback control: selectively reduce the villus cell population, for example by limited irradiation or ischaemia, and there is a compensatory 'surge' in Crypt cell proliferation [2]. Above this intrinsic mechanism stand other powerful influences that operate when the gut adapts to altered diet or surgical shortening. The small bowel has a great capacity to grow in response to partial tissue loss. The compensatory response involves all coats of the gut and probaLly all cell types. Functional improvement is simply achieved by greater numbers of newly-produced cells, which are individually immature [2,11]. Adaptive hyperplasia expla ins why patients can survive subtotal enteric resection or bypass and hope to return to near-normal patterns of eating, as diarrhoea subsides. Adaptation is governed largely by luminal factors, such as nutrients and endogenous secretions (e.g. bile, pancreatic juice), and partly by systemic factors, such as enteroglucagon [2,11]. Parenteral nutrition can be used experimentally to show whether the hypoplastic changes of fasting reflect a generalised catabolic reaction or the specific absence of nutrients from the gut. In several different species including man, total parerneraI nutrition has been shown to provide no protection whatsoever against the atrophic effects of starvation on the stomach, intestine and pancreas [15]. It does not even permit the small bowel to adapt to partial excision or exclusion [15,16]. Once again it is the jejunum that bears the brunt of hypoplasia in animals fed intravenously [ 17]. To the contrary, elemental diets appear to allow normal and adaptive growth of the upper alimentary tract but they cause colonic atrophy, presumably because they leave no residual bulk [10,15]. The clinical message is clear: a rested gut is an atrophic gut. Food is essential for healthy intestinal mucosa. Oral nutrients act in part by direct stimulation of mucosal growth and in part by releasing alimentary juices and hormones that have a tropic action. Parenteral nutrition" @default.
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• W2066476087 date "1984-12-01" @default.
• W2066476087 modified "2023-10-18" @default.
• W2066476087 title "Disuse atrophy of the intestinal tract" @default.
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• W2066476087 doi "https://doi.org/10.1016/s0261-5614(84)80039-4" @default.
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