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Original Article

Facilitating Effect of Amino Acids on Fructose and Sorbitol Absorption in Children

Hoekstra, J. Hans; van den Aker, Janet H. L.

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Journal of Pediatric Gastroenterology & Nutrition: August 1996 - Volume 23 - Issue 2 - p 118-124
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Several investigators, using breath H2 tests for the demonstration of incomplete absorption, have observed limited small intestinal uptake of fructose given as a single dose in adults (1,2) and children (3,4). Unlike free fructose, the fructose moiety in the disaccharide sucrose is well-absorbed, and so is fructose when ingested with an equimolar amount of glucose (2,3,5) or galactose (3). At the moment, the mechanism of this facilitating effect of glucose on fructose absorption, which is dose-dependent (2,3,6), is not adequately understood. In rats, the study of Fujisawa et al. suggested that equal quantities of fructose and glucose (or galactose) could use a sucrase-related transport system; acarbose, a blocker of brush-border α-glucosidases, inhibited the glucose-facilitated fructose absorption (7). An alternative explanation is that, under these circumstances, fructose profits from the water movement caused by the uptake of glucose through the well-defined glucose-transport systems, especially the glucose-Na+ cotransporter.

Sorbitol, which is also a part of natural foods, is incompletely absorbed at a rate much slower than that of fructose (8). When sorbitol is given as a single oral dose, the intestinal absorptive capacity has been estimated to be no more than 2-10 g (9-12); furthermore, it has been suggested that, when given together, sorbitol and fructose compete for absorption (12). As perfusion studies have indicated similar kinetics of absorption (8), Rumessen and Gudmand-Høyer suggested a common carrier for fructose and sorbitol (12). In one study, sorbitol absorption was shown to be enhanced by glucose (13), but these results were disputed (14).

The present study was conducted to investigate more closely the mechanisms influencing fructose and sorbitol absorption. We reasoned that acarbose could be used to ascertain the existence of a sucrase-related transport system in humans (7). On the other hand, if the effect of glucose on absorption is mediated by water movement, amino acids should show similar effects (15). Such studies have not previously been performed in humans.


The study group consisted of 15 randomly selected healthy children who had no history of GI symptoms or recent therapy with antibiotics or laxatives. All participated in a number of tests recording breath H2 excretion as an indicator of carbohydrate malabsorption following ingestion of various combinations of sugars and amino acids. The amino acids used were those that are absorbed through Na+ -coupled transport systems: L-alanine, L-phenylalanine, L-glutamine, and L-proline, all of which are transported by separate systems (16).

To limit the number of tests per child—and because the adverse effects of sorbitol and acarbose, that is, diarrhea and abdominal pain, could be a greater problem in younger children—we choose to perform some tests in well-informed older children only. The fructose tests were confined to the younger children because of their anticipated higher H2 production (4). Three groups were created (Table 1).

Group I

Group I consisted of five older children (two boys, three girls; age, 11.1-18.2 years; mean, 14.6).

For the sorbitol, sorbitol-fructose, sorbitol-glucose, and sorbitol-alanine tests, 10 g of sorbitol 20% was given separately and in combination with a deliberate fivefold excess of the other component of the mixture: 55 g of glucose 20% (equimolar to 50 g of fructose), 27.5 g of L-alanine (equimolar to 50 g of fructose), or 50 g of fructose 20%.

For the acarbose-sucrose and acarbose-fructose-glucose tests, tablets containing 200 mg of acarbose (Glucobay, Bayer Pharmaceutical Company, Wuppertal, Germany) were chewed and swallowed immediately before the ingestion of the test solutions, which contained either 47 g of sucrose 20% (equimolar to 25 g of fructose) or 25 g of fructose 20% plus 27.5 g of glucose 20%.

Group II

Group II included 10 children (five boys, five girls; age, 1.6-8.3 years; mean, 5.3).

For the fructose, fructose-glucose, and fructose-alanine tests, all children were given 2 g/kg of fructose 20% (maximum of 37.5 g), alone and in combination with equimolar amounts of glucose or L-alanine—i.e., 2.2 g/kg of glucose 20% or 1 g/kg of L-alanine 20%.

Group IIa

Five of the children in group II (group IIa) were also tested with 2 g/kg of fructose 20% in combination with alanine 20% at half of the original dose (0.5 g/kg) or with L-glutamine 20% in an equimolar amount (1.6 g/kg).

Group IIb

The other five children of group II (group IIb) were tested with 2 g/kg of fructose 20% in combination with equimolar amounts of L-phenylalanine 20% (1.85 g/kg) or L-proline 20% (1.3 g/kg).


All amino acids were obtained from Merck (Darmstadt, Germany). After an overnight fast of at least 10 h, a breath H2 test was performed after the subject drank one of the test solutions (in random order), with at least 2 days between tests. Before ingestion and at 30-min intervals thereafter, end-expiratory 20-ml breath samples were collected in duplicate. The total sampling time was 180 min in group I and 150 min in group II. H2 was estimated using the Lactoscreen breath tester (Hoek Loos, Rotterdam, The Netherlands), which measures H2 content of samples with an accuracy of 1 ppm. A breath H2 increase of ≥20 ppm over basal values was considered indicative of incomplete absorption. During the test and for 4 h thereafter, the children or their parents were asked to record any symptoms of diarrhea, gas, bloating, or cramps.

The studies were approved by the local ethical committee. Informed written consent was obtained from the parents. The results are expressed as means ± SD as well as 95% confidence intervals (CIs). Statistical analysis was done with the Student t test for paired data (two-sided).


Group I

Sorbitol Tests

Sorbitol ingestion resulted in H2 production in all children tested, as witnessed by peak H2 concentrations of 115 ± 54 ppm (95% CI, 47-182; Fig. 1). The addition of glucose to the sorbitol solution resulted in significantly lower peak H2 concentrations (42 ± 25 ppm; 95% CI, 11-74); this effect was even more pronounced in the L-alanine-containing solution (7 ± 5 ppm; 95% CI, 1-13; Fig. 1). Figure 2 illustrates breath H2 excretion following the three test solutions as a function of time. At the end of the test, breath H2 concentrations were significantly lower in the sorbitol-L-alanine solution than in the sorbitol-glucose solution. The H2 responses obtained following ingestion of the sorbitol-fructose solution were higher than those following sorbitol, but the difference did not reach significance. Adverse reactions to the solutions were only noted in two children following the sorbitol-fructose mixtures; they experienced abdominal discomfort and diarrhea.

Acarbose Tests

Acarbose pretreatment resulted in positive breath H2 tests in all children following the sucrose solution (62 ± 18 ppm) but not the fructose-glucose solution (2 ± 1 ppm; Fig. 3). The acarbose-sucrose tests caused mild symptoms with abdominal pain, flatulence, and diarrhea in all five children tested, while no problems were noted with the acarbose-fructose-glucose solution.

Group II

Fructose Tests

All 10 children had positive fructose breath H2 tests (68 ± 38 ppm; 95% CI, 41-95); glucose addition resulted in a significant decrease of breath H2 excretion (8 ± 10 ppm; 95% CI, 1-15; Fig. 4). An even more positive effect on fructose absorption was obtained with the addition of an equimolar dose of L-alanine (3 ± 3 ppm; 95% CI, 1-5; Fig. 4). On further evaluation, with tests performed in five children each, the solution containing half of the previous L-alanine dose was shown to promote fructose absorption as well (17 ± 4 ppm; 95% CI, 12-22), as did the other amino acids tested: L-glutamine (21 ± 12 ppm; 95% CI, 6-36), L-phenylalanine (8 ± 9 ppm; 95% CI, 0-19), and L-proline (19 ± 16 ppm; 95% CI, 0-39; Fig. 5). For all of these experiments, symptoms were only noted following the ingestion of the fructose solution, with six children experiencing mild abdominal symptoms with pain and diarrhea.


In the human diet, fructose is present mainly as a constituent of the disaccharide sucrose (17). In its free form, fructose is present in fruits, vegetables, and honey (18). Due to the development of an inexpensive industrial process for enzymatic conversion of corn starch into fructose, high-fructose corn syrups are used as sweeteners in soft drinks and other commercial food products. The Western diet includes an increasing amount of industrially added sugars and a growing percentage of free fructose (19,20). The notion that fructose absorption is far more limited than absorption of glucose and galactose is recent (1,3). Fructose malabsorption has been suggested to be a cause of chronic nonspecific diarrhea in toddlers (21). Interestingly, the degree of fructose malabsorption seems to be higher in this age group (4).

Sorbitol is also a natural constituent of several foods, including certain fruits and fruit juices, but the average daily intake from natural sources has been estimated to be as low as 0.2 g (22). As sorbitol, like xylitol, is a very popular sweetener in so-called sugar-free food products, the actual daily intake can mount to 10 g or more. Sorbitol, which is believed to be absorbed through a passive mechanism (8,13), may also cause abdominal pain and diarrhea in children (23,24) and adults (9,10).

The absorption of fructose was the subject of extensive studies in laboratory animals in the 1970s (25-28). Fructose was shown to be absorbed at rates faster than could be accounted for by passive diffusion alone, and an Na+-independent carrier-mediated mechanism was suggested (25-29). In recent years, strong evidence has been produced that fructose enters the cell through GLUT5, a specific fructose transporter expressed on the apical membranes of the enterocytes in the human small intestine (29-31). However, sucrose and fructose-glucose breath H2 tests have been interpreted to suggest a different pathway for fructose absorption. The presumed disaccharidase-related, high-capacity, glucose-dependent fructose cotransport mechanism (2,3) could represent a logical adaptation in the course of human evolution as fructose and glucose occur together in many natural food products.

It has been shown that diets high in sucrose and diets high in fructose increase human jejunal disaccharidase activity (32). Acarbose is a competitive inhibitor of small intestinal α-glucosidase. It interferes with the digestion of sucrose and starch (33) without affecting glucose absorption (34). In the rat, sucrase isomaltase inhibition by acarbose was shown to counteract the facilitating effect of glucose on fructose absorption, but the ensuing H2 production was highly variable and decreased with repeated administration of the test solutions to the same animal, necessitating the use of a different group of animals for each experiment (7). In contrast to these results obtained in rats, our results clearly show that in children, acarbose pretreatment has no effect on fructose absorption from a fructose-glucose solution, which is against the theory of a disaccharidase-related transport system for combinations of fructose and glucose.

As sorbitol is absorbed at slower rates than is fructose, we deliberately used a higher-than-equimolar dose of glucose to study its influence on sorbitol uptake. Thus, sorbitol absorption is stimulated by the presence of glucose in a similar way as occurs with fructose. Beaugerie et al. (13) studied sorbitol absorption in vivo with high luminal glucose concentrations, using human jejunal tissue preparations mounted in Ussing chambers. Their results are in accordance with our data. Since, in addition we found (not significantly) higher breath H2 excretion with the sorbitol-fructose solution than with sorbitol alone, our findings tend to underline the suggestion of Rumessen and Gudmand-Høyer (12) concerning competition for the same transport mechanism between fructose and sorbitol. In this respect, it would be very interesting to know whether GLUT5 is involved in sorbitol transport.

Our experiments investigating the effects of equimolar solutions of amino acids on fructose (and sorbitol) absorption provide an alternative explanation for the facilitating effect of glucose. We suggest that the facilitating effects of glucose as well as of amino acids on both fructose and sorbitol absorption are a consequence of the water flow through the apical membrane, which is generated by Na+-coupled substrate transport (35). On one hand, there is the so-called solvent drag, the force that requires that water and solute (i.e., fructose) traverse the mucosa through the same pathway (35). On the other hand, the increase in intraluminal fructose concentration caused by water removal from the lumen, also caused by actively absorbed substrates, might lead to increased transport of fructose. These two mechanisms together have recently been shown to account for 99% of glucose-stimulated D-xylose absorption (35). Therefore, the previously established dose-related enhancement of fructose transport by glucose would not be explained by a direct molecular relationship but by the fact that the increases in water flux also are dose-dependent.

Most amino acids are transported at the apical membrane by Na+-dependent carriers that are distinct from the monosaccharide-Na+ cotransport carrier (16,36,37). Both glucose and amino acid absorption, therefore, result in important water movement (15). The effects on water flow of alanine and glycine addition to oral rehydration solutions has been tested extensively in animals (38,39) and in humans (40,41). Both amino acids have a similar promoting effect on water absorption. The passage of amino acids from the small intestinal lumen to the blood involves transport through apical and basolateral membranes as well as paracellular routes (37). Multiple pathways have been established with different specificities (16,36,42). The L-alanine transporter is the Na+-dependent apical NBB system, which is responsible for the majority of neutral amino acids (43). Another transporter, the PHE system, which is less active than the NBB system, is responsible for the uptake of the neutral amino acid L-phenylalanine (42). The Na+-dependent IMINO carrier is highly specific for L-proline transport, but it too is less active than the NBB system (43). Finally, L-glutamine, which is the primary metabolic fuel for the enterocyte, is efficiently absorbed by the human small intestine with kinetic parameters approaching those of glucose (44). In contrast to alanine, glutamine equally stimulates electrogenic and electroneutral NaCl absorption (45).

Although it is clear that the active mucosal transport of these amino acids results in substantive water absorption, there are no data available with regard to the relative efficacy of the various amino acids. There may be a general rule that amino acids absorbed at higher rates result in the absorption of more water. This would be in accordance with our finding that L-alanine improves fructose absorption better than other amino acids do and that L-alanine has an even more profound effect on the absorption of fructose and sorbitol than has glucose. As is shown in Figs. 2 and 4, which exhibit breath H2 excretion as a function of time, glucose addition results in a minor peak at the end of the test that is not seen with L-alanine. An additional explanation for this difference may be found in the absorption profiles of glucose and L-alanine, as protein (42,46) and amino acid absorption (42) is more evenly distributed along the whole of the small intestine than is glucose absorption, supporting fructose absorption over a longer distance.

Theoretically, the inhibition of H2 production by the colonic flora in the presence of L-alanine, which in this dose might be incompletely absorbed, could be an alternative explanation for the lack of H2 response following the fructose-L-alanine mixture, In healthy adults, however, 27.5 g of L-alanine did not prevent the increase in breath H2 excretion following ingestion of 20 g of lactulose (unpublished observations), which excludes such a mechanism.

In conclusion, our results cast doubt on the existence of a sucrase-related fructose-transport system as an explanation for glucose-facilitated fructose absorption. It would rather seem that the enhancing effect of glucose is nonspecific as it is exhibited also by amino acids. The enhancement could therefore be better explained by the effects of water movement across the brush border induced by Na+-coupled substrate transport, either due to pure “solvent drag” or to a positive influence on fructose transport. The nonspecific nature of this kind of facilitation could also help to explain the fate of fructose and sorbitol in human nutrition, because it would explain why both sorbitol and fructose are better absorbed when given in a meal than in a solution (47).

Acknowledgment: We thank Gerald Staaks for technical support and Dr. C. M. Frank Kneepkens (Amsterdam, The Netherlands) for critically reviewing the manuscript. This study was supported by a grant from the Peribosch Foundation.

FIG. 1.
FIG. 1.:
Mean ± SD of peak breath H2 increases (ppm) in group I after ingestion of 10 g sorbitol and in combination with 55 g of glucose or 25 g of L-alanine. A rise over baseline of 20 ppm or more was considered to indicate malabsorption. Sorbitol absorption was facilitated in the presence of glucose (sorbitol vs. sorbitol-glucose, p ≤ 0.05) and L-alanine (sorbitol vs. sorbitol-alanine, p ≤ 0.01; sorbitol-glucose vs. sorbitol-alanine, p ≤ 0.05). Peak breath H2 concentrations were higher following the sorbitol-fructose solution than following sorbitol, but the difference was not significant (p = 0.08). (S, sorbitol; G, glucose; Al, alanine; F, fructose.)
FIG. 2.
FIG. 2.:
Breath H2 profiles (ppm; mean ± SD) over time of the tests presented in Fig. 1. At 60, 90, 120, 150, and 180 min, breath H2 concentrations were lower with glucose and L-alanine added (p ≤ 0.05). At 150 min, L-alanine addition resulted in lower breath H2 concentrations than did glucose addition (p ≤ 0.05). Test solutions contained 10 g of sorbitol (white circles), 10 g of sorbitol plus 50 g of glucose (black circles), or 10 g of sorbitol plus 25 g of L-alanine (squares).
FIG. 3.
FIG. 3.:
Breath H2 increases (ppm) in acarbose-pretreated children (group I) after ingestion of sucrose and fructose-glucose solution. After acarbose pretreatment, all subjects ingesting sucrose displayed malabsorption (peak H2 concentration, mean ± SD, 62 ± 18 ppm), in contrast to findings with the fructose-glucose solution (2 ± 1 ppm; p ≤ 0.0005).
FIG. 4.
FIG. 4.:
Breath H2 profiles over time in group II after ingestion of 2 g/kg of fructose separately (white circles) and in combination with equimolar amounts of glucose (black circles) and L-alanine (squares). At 30, 60, 90, 120, and 150 min, mean breath H2 concentrations in the glucose and L-alanine tests were lower than with fructose alone (p ≤ 0.05). At 150 min, there was a significant (p ≤ 0.05) difference between the fructose-L-alanine and fructose-glucose solutions.
FIG. 5.
FIG. 5.:
Mean peak breath H2 increases (ppm) in group II following the ingestion of 2 g/kg of fructose alone and in combination with equimolar amounts of glucose and L-alanine. Children of group IIa had further tests with, in addition to fructose, half of the previously given amount of L-alanine and an equimolar amount of L-glutamine. Children of group IIb were further tested with, in addition to fructose, equimolar amounts of L-phenylalanine and L-proline. Peak breath H2 concentrations were lower in solutions containing glucose (p ≤ 0.005) and, even more pronounced, in solutions containing L-alanine (p ≤ 0.001; fructose-glucose vs. fructose-alanine, p ≤ 0.05). All tests in group II resulted in increased fructose absorption compared with fructose given alone (p ≤ 0.05 for each combination separately). Due to the small number of tests, the differences between fructose-alanine and fructose-alanine (half dose), fructose-proline, and fructose-glutamine failed to reach significance (p = 0.05-0.10). (F, fructose; G, glucose, AI, alanine; 0.5AI, half dose of alanine; Glut, glutamine; Phen, phenylalanine; Prol, proline.)


1. Ravich WJ, Bayless TM, Thomas M. Fructose: incomplete intestinal absorption in humans. Gastroenterology 1983;84:26-9.
2. Rumessen JJ, Gudmand-Høyer E. Absorption capacity of fructose in healthy adults. Comparison with sucrose and its constituent monosaccharides. Gut 1986;27:1161-8.
3. Kneepkens CMF, Vonk RJ, Fernandes J. Incomplete intestinal absorption of fructose. Arch Dis Child 1984;59:735-8.
4. Hoekstra JH, van Kempen AAMW, Bijl SB, Kneepknes CMF. Fructose breath hydrogen tests. Arch Dis Child 1993;68:136-8.
5. Holdsworth CD, Dawson AM. The absorption of monosaccharides in man. Clin Sci 1964;27:371-9.
6. Truswell AS, Seach JM, Thorburn AW. Incomplete absorption of pure fructose in healthy subjects and the facilitating effect of glucose. Am J Clin Nutr 1988;48:1424-30.
7. Fujisawa T, Riby J, Kretchmer N. Intestinal absorption of fructose in the rat. Gastroenterology 1991;101:360-7.
8. Mehnert H, Stuhlfauth K, Mehnert B, Lausch R, Seitz W. Vergleichende Untersuchungen zur Resorption von glucose, fructose und sorbit beim Menschen. Klin Wochenschr 1959;37:1138-42.
9. Hyams JS. Sorbitol intolerance: an unappreciated cause of functional gastrointestinal complaints. Gastroenterology 1983;84:30-3.
10. Jain NK, Rosenberg DB, Ulahannan MJ, Glasser MJ, Pitchumoni CS. Sorbitol intolerance in adults. Am J Gastroenterol 1985;80:678-81.
11. Rumessen JJ, Gudmand-Høyer E. Functional bowel disease: malabsorption and abdominal distress after ingestion of fructose, sorbitol and fructose-sorbitol mixtures. Gastroenterology 1988;95:694-700.
12. Rumessen JJ, Gudmand-Høyer E. Malabsorption of fructose-sorbitol mixtures. Interactions causing abdominal distress. Scand J Gastroenterol 1987;22:431-6.
13. Beaugerie L, Nath SK, Desjeux JF. Le glucose stimule l'absorption du sorbitol à travers la muqueuse jéjunale humaine. Gastroenterol Clin Biol 1989;13:379-82.
14. Born P. Absorption of sorbitol: facilitating effect of glucose [Letter]? Gastroenterol Clin Biol 1991;15:261.
15. Hellier MD, Thirumalai C, Holdsworth CD. The effect of amino acids and dipeptides on sodium and water absorption in man. Gut 1973;14:41-5.
16. Argiles JM, Lopez-Soriano J. Intestinal amino acid transport: an overview. Int J Biochem 1990;9:931-7.
17. Glinsmann WH, Irausquin H, Park YK. Evaluation of health aspects of sugars contained in carbohydrate sweeteners. J Nutr 1986;116(11S):S1-216.
18. Hardinge MG, Swarner JB, Crooks H. Carbohydrates in foods. J Am Diet Assoc 1965;46:197-204.
19. Rugg-Gunn AJ, Hackett AF, Appleton DR, Moynihan PJ. The dietary intake of added and natural sugars in 405 english adolescents. Hum Nutr Appl Nutr 1986;40A:115-24.
20. Park YK, Yetley EA. Intakes and food sources of fructose in the United States. Am J Clin Nutr 1993;58:737S-47S.
21. Kneepkens CMF, Jakobs C, Douwes AC. Apple juice, fructose and chronic nonspecific diarrhoea. Eur J Pediatr 1989;148:571-3.
22. Wang YM, van Eijs J. Nutritional significance of fructose and sugar alcohols. Annu Rev Nutr 1981;1:437-75.
23. Gryboski JD. Diarrhea from dietetic candies. N Engl J Med 1966;275:718.
24. Hyams JS. Chronic abdominal pain caused by sorbitol malabsorption. J Pediatr 1982;100:772-3.
25. Schultz SG, Strecker CK. Fructose influx across the brush border of rabbit ileum. Biochim Biophys Acta 1970;211:586-8.
26. Guy MJ, Deren JJ. Selective permeability of the small intestine for fructose. Am J Physiol 1971;221:1051-6.
27. Sigrist-Nelson K, Hopfer U. A distinct D-fructose transport system in isolated brush border membrane. Biochim Biophys Acta 1974;367:247-54.
28. Macrae AR, Neudoerffer TS. Support for the existence of an active transport mechanism of fructose in the rat. Biochim Biophys Acta 1972;288:137-44.
29. Davidson NO, Hausman AM, Ifkovits CA, et al. Human intestinal glucose transporter expression and localisation of GLUT5. Am J Physiol 1992;262:C795-800.
30. Burant CF, Takeda J, Brot-Laroche E, Bell GI, Davidson NO. Fructose transporter in human spermatozoa and small intestine is GLUT5. J Biol Chem 1992;267:14523-6.
31. Rand EB, Depaoli AM, Davidson NO, Bell GI, Burant CF. Sequence, tissue distribution, and functional characterization of the rat fructose transporter GLUT5. Am J Physiol 1993;264:G1169-76.
32. Rosenzweig NS, Herman RH. Control of jejunal sucrase and maltase activity by dietary sucrose and fructose in man. J Clin Invest 1968;47:2253-62.
33. Ruppin H, Hagel J, Feuerbach W, et al. Fate and effects of the α-glucosidase inhibitor acarbose in humans. Gastroenterology 1988;95:93-9.
34. Jenkins DJA, Taylor RH, Goff DV, et al. Scope and specificity of acarbose in slowing carbohydrate absorption in man. Diabetes 1981;30:951-4.
35. Fine KD, Santa Ana CA, Porter JL, Fordtran JS. Mechanism by which glucose stimulates the passive absorption of small solutes by the human jejunum in vivo. Gastroenterology 1994;107:389-95.
36. Hopfer U. Membrane transport mechanisms for hexoses and amino acids in the small intestine. In: Johnson LR, ed. Physiology of the gastrointestinal tract. 2nd ed. New York: Raven Press, 1987:1499-526.
37. Desjeux JF, Tannenbaum C, Tai Y-H, Curran PF. Effects of sugars and amino acids on sodium movement across small intestine. Am J Dis Child 1977;131:331-40.
38. Cunha Ferreira RMC, Elliott EJ, Watson AJM, Brennan E, Walker-Smith JA, Farthing MJG. Dominant role for osmolality in the efficacy of glucose and glycine containing oral rehydration solutions: studies in a rat model of secretory diarrhoea. Acta Paediatr 1992;81:46-50.
39. Rhoads JM, MacLeod RJ, Hamilton JR. Alanine enhances jejunal sodium absorption in the presence of glucose: studies in piglet viral diarrhea. Pediatr Res 1986;20:879-83.
40. Nalin DR, Cash RA, Rahman M, Yunus MD. Effect of glycine and glucose on sodium and water absorption in patients with cholera. Gut 1970;11:768-72.
41. Da Costa Ribeiro H, Lifshitz F. Alanine-based oral rehydration therapy for infants with acute diarrhea. J Pediatr 1991;118:S86-90.
42. Malo C. Multiple pathways for amino acid transport in brush border membrane vesicles isolated from the human fetal small intestine. Gastroenterology 1991;100:1644-52.
43. Stevens BR, Kaunitz JD, Wright EM. Intestinal transport of amino acids and sugars: advances using membrane vesicles. Annu Rev Physiol 1984;46:417-33.
44. Déchelotte P, Darmaun D, Rongier M, Heckelsweiler B, Rigal O, Desjeux JF. Absorption and metabolic effects of enterally administered glutamine in humans. Am J Physiol 1991;260:G677-82.
45. Rhoads JM, Keku EO, Woodward JP, Bangdiwale SI, Lecce JG, Gatzy JT. L-Glutamine with D-glucose stimulates oxidative metabolism and NaCl absorption in the piglet jejunum. Am J Physiol 1992;263:G960-6.
46. Silk DBA, Dawson AM. Intestinal absorption of carbohydrate and protein in man. In: Crane RK, ed. International review of physiology. Volume 19. Gastrointestinal physiology III. Baltimore: University Park Press, 1979:151-204.
47. Zeitoun E, Flourié B, Beaugerie L, et al. Influence of a meal on the intestinal absorption of a sugar alcohol. Gastroenterology 1993;104:A655.

Fructose; Sorbitol; Amino acids; Transport facilitation; Acarbose; Breath hydrogen test

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