Role of Oral Intake in Maintenance of Gut Mass and Disaccharide Activity

Previous studies demonstrating small intestinal atrophy and hypoplasia during fasting failed to distinguish between negative nitrogen balance and lack of oral intake as the cause for the observed changes. To differentiate between these factors, intravenously alimented (IVA) rats were compared with r...

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Veröffentlicht in:Gastroenterology (New York, N.Y. 1943) N.Y. 1943), 1974-11, Vol.67 (5), p.975-982
Hauptverfasser: Levine, Gary M., Deren, Julius J., Steiger, Ezra, Zinno, Ronald
Format: Artikel
Sprache:eng
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Zusammenfassung:Previous studies demonstrating small intestinal atrophy and hypoplasia during fasting failed to distinguish between negative nitrogen balance and lack of oral intake as the cause for the observed changes. To differentiate between these factors, intravenously alimented (IVA) rats were compared with rats fed the same solution orally (OA). After 1 week, decreases in gut weight (22%), mucosal weight (28%), mucosal protein (35%), DNA (25%), and mucosal height were observed in IVA rats, primarily due to a decrease in these parameters in the proximal small bowel. As a result of the atrophy and hypoplasia of the proximal gut, the proximal to distal gradient of mass, protein, and DNA observed in OA rats was minimal after IVA. IVA rats had lower total intestinal maltase (62%), sucrase (62%), and lactase (44%), with a 46% decrease in maltase and sucrase specific activities, but without a change in lactase specific activity. Sucrase and maltase activities (specific activity and per centimeter) were highest in the jejunum of both groups, although they were higher in OA than in IVA rats. Lactase activity per centimeter was greater in OA rats, reflecting the greater protein content, but without a change in specific activity. This study demonstrates that the physiological responses related to food ingestion are important in maintaining small intestinal mass, disaccharidase activity, and the proximal-distal gradient.
ISSN:0016-5085
1528-0012
DOI:10.1016/S0016-5085(19)32752-0