Lactase Specific Activity Research Articles

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 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.

Effect of prolonged fasting on fatty acid re-esterification in rat intestinal mucosa

Rats subjected to a three day fast showed marked decreases in total intestinal mucosal protein, mucosal weight, sucrase, maltase and monoacylglycerol acyltransferase activities. Total microsomal protein was decreased to a lesser degree in fasted rats, and total lactase activity remained unchanged. Specific activities of sucrase and maltase were unchanged by fasting; specific activity of lactase increased. Specific activity of monoacylglycerol acyltrans-ferase, expressed per mg microsomal protein decreased. When activity of this pathway was expressed per mg of mucosal protein or mucosal weight it remained unchanged in fasted animals. The results appeared most consistent with the hypothesis of decreased cell proliferation in starvation. A change in the usual proportions of cell types during starvation is also suggested.

The development of some digestive enzymes in the intestines of pigs reared artificially

SUMMARYA comparison was made of the development of acid and alkaline phosphatase, invertase, lactase and leucine aminopeptidase specific activities in the small intestines of two groups of neonatal pigs. The groups consisted of two litters of suckling pigs and two litters of pigs that were delivered by hysterectomy and reared in incubators on a diet based on cow's milk. In the unsuckled pigs there was retardation of the development of invertase and leucine aminopeptidase. The unsuckled animals grew slowly and were affected by diarrhoea, and it is possible that enteric disease may have affected the development of the brush border of the intestinal epithelial cells, or enzymes specifically associated with the microvilli.

THE EFFECT OF FASTING ON DISACCHARIDASE ACTIVITY IN THE RAT SMALL INTESTINE

We assessed intestinal structure, mucosal epithelial kinetics, and disaccharidase activities after fasting. Rats fasted for up to 120 hours were compared with control rats fed ad libitum. All rats had free access to water and all were prevented from ingesting their own stools. Body weight, small intestinal weight and mucosal protein, and maltase and sucrase activity of the total small intestine decreased in fasted rats. Lactase activity did not decrease. Specific activity of lactase actually increased in the jejunum. Assessed after a 96-hour fast, jejunal villi were shortened with less epithelial cells along their length and the rate of migration of those cells along the villi was diminished in the fasted rats compared with control rats. We attribute the decreased total intestinal sucrase and maltase activities to a loss of total epithelial cell mass in the small bowel. An abnormality in the cells of the progenitor zone of the crypts is suggested by the decreased migration rate of mucosal epithelial cells in fasting rats. These factors do not explain our observations completely since lactase activity did not diminish. We postulate that the activity of the "acid" β-galactosidase located in the cytoplasm or lysosomes of the epithelial cells was stimulated by fasting. Our observations are relevant to clinical pediatrics. Undernutrition and fasting my be associated with many childhood diseases and with treatment of disease. In assessing clinical data and advising treatment, the pediatrician should be aware of the potentially harmful effects of starvation on intestinal structure and function.