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This study was undertaken to assess the short-term effects of EGF on sodium and glucose uptake, glucose metabolism and Na+/K(+)-ATPase activity in isolated enterocytes of rats. Jejunal cells exposed to EGF had a significantly greater total uptake of sodium compared to controls after 6 min. Kinetic analysis of glucose transport across BBMV's demonstrated similar Km values but a significant increase of the Vmax in vesicles prepared from cells first exposed to EGF as compared to controls. EGF was also associated with a significant increase in glucose metabolism of jejunal enterocytes after 15 min. The activity of Na+/K(+)-ATPase increased in jejunal enterocytes exposed to EGF. The increase in Na+/K(+)-ATPase activity of the cells following EGF exposure was not accompanied by an increase in immunodetectable total or assembled Na+/K(+)-ATPase protein. EGF's effect on enzyme activity was abolished by removing NaCl from the incubation solution, and by preincubating the enterocytes with phlorizin prior to addition of EGF. Preincubation with amiloride did not inhibit the effect of EGF on Na+/K(+)-ATPase. The results confirm that EGF promotes uptake of both sodium and glucose by the jejunal mucosal cells, and suggest the effect of EGF on glucose and sodium is mediated through the brush-border membrane glucose-sodium transporter. The increase in Na+/K(+)-ATPase activity that occurs with EGF appears to be secondary to a rise in intracellular Na+ concentration. The short-term effects of EGF on glucose and sodium transport by the small intestine may have potential therapeutic implications.

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To determine the prevalence of short polymers of glucose and starch malabsorption caused by small intestinal glucoamylase deficiency in children with chronic diarrhea, we studied small bowel biopsy specimens from 511 children (aged 1 month to 9 years) with chronic diarrhea evaluated at 54 medical centers. Glucoamylase and disaccharidase (lactase, sucrase, maltase, and palatinase) enzyme assays were performed. Of the 511 children, 15 had glucoamylase deficiency. Six who had significant small intestinal mucosal injury and disaccharidase deficiencies were defined as having secondary glucoamylase deficiency; the other nine patients with normal mucosal morphologic features were defined as having primary glucoamylase deficiency. Secretin tests showed normal pancreatic amylase values for age in all seven children tested. Four of them had abnormal findings on tolerance tests for starch and short polymers of glucose (rise in blood glucose concentration: < 20 mg/dl) and reducing substances in stools, and three of these four had symptoms of intolerance (abdominal distention, flatulence, and diarrhea). All seven patients responded to a starch elimination diet. After reintroduction of a starch diet, diarrhea recurred in four patients; this was alleviated 48 hours after reelimination of starch. We conclude that intestinal glucoamylase deficiency is present in some patients with chronic diarrhea.

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Several issues involving glucose-based oral rehydration therapy may limit its acceptability and sustained use. Our studies suggest that defined short-chain glucose polymers (2 to 9 glucose units) are hydrolyzed and absorbed faster than isocaloric solutions of D-glucose in the small intestine of the rat. Glucose polymers, primarily from rice-based solutions, have been shown to be as effective as glucose-based solutions. They offer additional advantages in reducing the amount and duration of diarrhea with lesser volumes of solution, thereby reducing the costs of treatment. Rice-based solutions provide high caloric density and increase the absorption of sodium without an osmotic overload. The result is increased net absorption of glucose, sodium, and water. Glucose polymers from rice or other starches in oral rehydration solutions may be effective, inexpensive, easily used, and safe treatments for acute diarrhea.

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Because rice remains the most available carbohydrate in developing countries, where chronic diarrhea is most prevalent, we compared the in vitro hydrolysis and clinical tolerance of rice glucose polymer with those of corn glucose polymer. Rice glucose polymer hydrolysis to D-glucose and short-chain polymers (polymers with two to four glucose units and those with five or more units) was similar to that for corn glucose polymers during incubation with saliva or duodenal aspirates. However, rice glucose polymers yielded more short-chain products than corn glucose polymers during incubation with pooled mucosal homogenates (p less than 0.01). In vivo tolerance testing of 16 infants with chronic diarrhea confirmed that rice glucose polymers were well tolerated and, compared with corn glucose polymers, achieved a higher maximal increase of serum glucose concentration (36.6 +/- 7.3 vs 27.6 +/- 10.3 mg/dl; p less than 0.02), a shorter time to peak serum glucose concentration (34.0 +/- 10.2 vs 52.5 +/- 25.7 minutes; p less than 0.02), and a greater area under the serum glucose response curve at 30 minutes (538 +/- 131 vs 1035 +/- 501 cm; p less than 0.02). We conclude that rice glucose polymers are rapidly hydrolyzed in vitro and in vivo and are more rapidly absorbed than are corn glucose polymers in children with chronic diarrhea.

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Urinary carnitine esters were quantitated in an infant with medium-chain acylcoenzyme A dehydrogenase deficiency by means of a highly sensitive and specific radioisotopic exchange high-pressure liquid chromatography method. During fasting, the excretion of free carnitine and of acetylcarnitine, octanoylcarnitine, and hexanoylcarnitine was increased. The fractional tubular reabsorption of free carnitine was decreased, suggesting a renal leak of free carnitine. In the symptom-free, fed state, only minor amounts of free carnitine and of short-chain acylcarnitine, octanoylcarnitine, and hexanoylcarnitine were present in urine, and carnitine loss occurred in the form of "other" carnitine esters not exceeding that of control subjects. During L-carnitine therapy, the excretion of free carnitine, short-chain acylcarnitine, octanoylcarnitine, and hexanoylcarnitine, and particularly of "other" carnitine esters, was increased, suggesting a possible detoxifying effect of administered carnitine that is not confined to the elimination of octanoic and hexanoic acids. The employed method detects very low urinary concentrations of octanoylcarnitine and hexanoylcarnitine (less than 1 mumol/L) characteristic of medium-chain acyl-coenzyme A dehydrogenase deficiency and may be useful in screening for this disease, which has been associated with sudden infant death.

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Using an enzyme-linked immunosorbent assay (ELISA) assay, we studied the sera of 17 patients with celiac disease and 114 control subjects for the levels of IgG and IgA antigliadin antibodies. As a group, the patients with celiac disease had significantly higher levels of antigliadin antibodies of both IgG and IgA classes (p less than or equal to 0.001). However, there was a significant overlap of values, resulting in respective sensitivities and specificities of 88% and 90% for IgG antigliadin antibodies, and 73% and 65% for IgA antigliadin antibodies. The combined use of both IgG and IgA antigliadin antibody levels produced a sensitivity of 86% and a specificity of 90%. A gluten-free diet in celiac patients did not seem to affect these results. We conclude that the antigliadin antibody ELISA assay cannot be used as a definitive diagnostic test for celiac disease. The small-bowel biopsy remains the principal diagnostic method; the ELISA assay should, at best, be considered a screening test for this disease.

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The interaction between malnutrition and exposure to a mucosal damaging agent, difluoromethylornithine (DFMO), was examined by monitoring the small-intestinal changes in weanling rats. Malnutrition as induced by the expanded-litter method resulted in severe reduction in body weights in the expanded litters as compared to normal litters. Subsequent treatment of malnourished and well-nourished pups with DFMO for 7 days resulted in decreases in small-intestinal weights and enzyme contents. A 2 factors (well-nourished and malnourished) by 2 factors (DFMO-treated and nontreated) analysis of variance showed no interaction between malnutrition and DFMO treatment in terms of food intake, total mucosal protein, and contents of enterokinase, leucine aminopeptidase and sucrase. Very slight and insignificant interactions (p less than or equal to 0.2) were found for body weights, intestinal weights and total DNA content. Only one parameter studied, the maltase content, showed significant interaction between malnutrition and DFMO treatment (p less than 0.05). Three weeks after the withdrawal of DFMO, essentially all the changes caused by DFMO recovered. But those changes caused by malnutrition did not, such that the malnourished group, whether treated with DFMO or not, still remained significantly less than the control group in their small-intestinal parameters. Analysis of variance showed no interaction between malnutrition and DFMO treatment in the recovery phase. The results suggest that malnutrition is a more important factor in determining the intestinal damage and that malnutrition in the immediate postnatal period does not increase the sensitivity of the small intestine to the damaging effect of DFMO.

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The role of caloric density in the regulation of gastric emptying has been well documented in adults but studied to only a limited extent in young infants. Ten premature infants were each fed 22 ml/kg formula (Similac Special Care), at concentrations of 24, 20, 13, and 6.5 Cal/oz, as well as one feeding of distilled water. The volume of gastric contents was measured at 20-minute intervals by the double-aspiration technique using the marker polyethylene glycol 4000. Analysis of variance demonstrated a significant inhibition of gastric emptying related to increasing caloric density (P less than 0.001) when evaluated over the entire time of measurement. By 20 minutes, significant differences (P less than 0.01) were present between 0 and 6.5, 6.5 and 13, and 13 and 20 Cal/oz. A volume difference between 20 and 24 Cal/oz (P less than 0.05) was present only at 80 minutes. Despite the inhibition of emptying, higher caloric density feedings were associated with emptying of more calories over comparable periods (P less than 0.001). Regulation of gastric emptying by caloric density in premature infants is qualitatively similar to that in adults.

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We evaluated the in vitro and in vivo digestibility and clinical tolerance of three corn syrup sugars (DE10, 15, 24) and one infant formula containing corn syrup sugar as the sole carbohydrate source (DE24). In vitro studies were conducted using human duodenal fluid and jejunal mucosa with normal enzyme activities. In vivo studies included intragastric perfusion studies and tolerance tests using the corn syrup sugars and a clinical formula trial in 32 infants with acute diarrhea. Results of the in vitro studies showed that each of the corn syrup sugars was well hydrolyzed by duodenal fluid and by mixtures of duodenal fluids and mucosal homogenates. Similarly, in vivo studies revealed significant hydrolysis in the proximal intestine, as measured during the perfusion studies, and adequate absorption, as indicated by a rise in serum glucose concentration during tolerance tests. Only patients who had a marginal serum glucose rise after a glucose meal had a blunted rise after a corn syrup feeding. More than 85% of the infants beginning the clinical trial tolerated the formula well and gained weight at or above the expected rate for age during the study interval. These data indicate that, except with severe mucosal injury and secondary monosaccharide intolerance, glucose polymers of the dextrose equivalents tested are suitable carbohydrate sources for infants recovering from acute diarrhea.

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We have described the developmental pattern of the gastrointestinal tract under optimal conditions (i.e., low risk pregnancy and normal labor and delivery at term). The tissues do not develop simultaneously, and morphologic and functional development are not concurrent. An important consideration is the effect of suboptimal or even adverse conditions on the developmental sequence and attainment of maturity. Malnutrition during both the prenatal and postnatal periods may restrict the morphologic and biochemical development of the gastrointestinal tract. Dietary modifications have been shown to alter the developmental pattern of intestinal and pancreatic enzymes in animal models. Drugs and hormonal therapy given during pregnancy and early infancy have been known to cause developmental defects, but the specific effects on the gastrointestinal tract have not been evaluated. For further understanding of digestibility of nutrients and absorption in the perinatal period, these departures from the normal development of the gastrointestinal tract and the mechanisms by which these potential effects occur remain to be described. In view of these undetermined factors, in the case of intolerance or unavailability of milk from the natural mother, feedings should be individualized, with attention to direct measurement of enzyme concentrations, balance studies, or both, especially in the case of extreme prematurity or unusual requirements.

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The development of glucoamylase activity was compared to that of disaccharidase in the small intestinal mucosa of infants and children. By the age of one month, infants have glucoamylase and disaccharidase levels comparable to those of young adults, indicating that young infants may be able to digest and absorb starches. In infants and children with varying degrees of mucosal injury of the small intestine, the activities of glucoamylase decreased progressively with increasing severity of the villus atrophy. However, the reduction of lactase, palatinase, and sucrase activities was more severe than the loss of activities of glucoamylase and maltase. Thus, children and infants may tolerate polymers of glucose better than disaccharides when they have mucosal injury associated with prolonged diarrhea.

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The disaccharidase activities in small intestinal biopsies were related to the morphology of the mucosa and the ages of 63 patients with cystic fibrosis and 177 healthy control subjects of Caucasian origin. In patients with CF and in the healthy control subjects under 5 years of age with normal intestinal mucosa, no low lactase activity was found. In those patients with CF who were over 5 years of age, one group had high and one group had low lactase activity, as occurs in healthy Caucasian control subjects of the same age. This finding supports the view that in patients with CF, lactase deficiency is not related to the disease entity. In patients with or without CF who had the same degree of mucosal atrophy, the decrease of disaccharidase activities followed the same pattern, indicating that enzyme activities are affected to the same extent by the damage of the mucosa. In patients with CF with pancreatic insufficiency, the disaccharidase activities were significantly (P less than 0.001) higher when compared to those in control subjects of the same age and ethnic group, although the increase was not uniform in all patients with cystic fibrosis.

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