Lactulose Feeding Lowers Cecal Densities of Clostridia in Piglets
| Autor: | Ruth Blauwiekel, Carol H. Williams, Randal K. Buddington, C. Lawrence Kien, Janice Y. Bunn |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2007 |
| Předmět: |
Diarrhea
030309 nutrition & dietetics Swine medicine.medical_treatment Inulin Laxative Colony Count Microbial Medicine (miscellaneous) Butyrate Biology Article Statistics Nonparametric Butyric acid 03 medical and health sciences chemistry.chemical_compound Lactulose Random Allocation 0302 clinical medicine Enteral Nutrition Gastrointestinal Agents Malabsorption Syndromes medicine Animals Food science Cecum Clostridium 0303 health sciences Gastrointestinal agent Nutrition and Dietetics Fructooligosaccharide Prebiotic Probiotics Organ Size Butyrates chemistry Animals Newborn 030211 gastroenterology & hepatology medicine.drug |
| Popis: | Because of our clinical interest in how to approach enteral feeding of patients with osmotic diarrhea secondary to carbohydrate malabsorption (and incomplete fermentation), we developed a piglet model of carbohydrate malabsorption: persistent feeding of lactulose, an indigestible disaccharide of galactose and fructose.1–3 Our research suggests that osmotic diarrhea caused by lactulose malabsorption has minimal, if any, clinical effects, but lactulose feeding consistently causes decreased cecal cell proliferation.1–3 Because, in vivo, butyrate produced by bacteria and well absorbed from the colonic lumen4 causes increased cell proliferation,5–7 we hypothesized that osmotic diarrhea might cause a form of in vivo butyrate deficiency, in part characterized by decreased cell proliferation in the colon.1 We then sought ways to enhance colonic fermentation so that when challenged with severe carbohydrate malabsorption, fermentation (and butyrate production) might be enhanced. Previously, others8 had shown that giving adult volunteers a prolonged, non-diarrheogenic dose of lactulose attenuated the subsequent diarrhea caused by a “laxative” dose of lactulose, and we theorized that augmenting the fermentation capacity with a fermentable carbohydrate other than lactulose might have a similar effect.1 Inulin is an indigestible and highly fermentable fructooligosaccharide (FOS), with an average of 35 fructosyl units. FOSs are found naturally in foods such as wheat, onion, and garlic, in an increasing number of processed foods used as low-energy, low-glycemic-index, noncariogenic sweeteners (functional foods), and in various formulas, cereals, and other foods for infants.4,9 In healthy adults, the threshold for diarrhea with FOS is about 55 g/d (0.8 g/kg/d).9 Inulin (3 g/L of formula, or about 0.4 g/kg/d) has been used by others to increase colonic cell proliferation in piglets.10 There is controversy about the extent to which feeding inulin enhances butyrate formation.3,10,11 In an initial study, we showed a trend in lactulose-treated piglets toward enhanced cecal cell proliferation and reduced diarrhea when inulin was prefed for 7 days and then discontinued before a challenge with lactulose.2 These results seemed consistent with our original hypothesis that fermentation and butyrate production were inhibited by high purging rates, but enhancing bacterial activity in the colon by prefeeding inulin could reverse these effects. In a subsequent study, we measured the rate of colonic luminal synthesis of butyric acid in growing, chronically catheterized piglets orally fed sow milk replacement formula, with or without supplements with lactulose, inulin, or inulin plus lactulose.3 We observed a doubling of the rate of butyrate synthesis in the group fed lactulose (15.2 g/kg/d)3; a combination of both prefeeding and then cofeeding inulin (0.4 g/kg/d) with lactulose (15.7 g/kg/d) prevented the decrease in cecal cell proliferation observed with lactulose feeding and was associated with normalization of butyrate synthesis.3 When compared with the control group, piglets fed inulin without lactulose (0.4 g/kg/d) manifested lower cecal cell proliferation, more diarrhea, and an intermediate rate of butyrate synthesis that was not statistically different from controls or lactulose-fed piglets.3 One hypothetical explanation for these data is that fructose-containing sugars, lactulose or inulin, exert a “prebiotic” effect,12 namely, suppression of growth of specific bacterial species, which via an independent, unknown mechanism normally stimulate cecal cell proliferation. However, when fed together, they may competitively inhibit the use of either sugar as a substrate for fermentation by this/these bacterial species, resulting in no change in cecal cell proliferation from normal.2,3 Butyrate synthesis, then, could be a function of the amount of fermentable sugar reaching the colon (much greater for lactulose in our model), rather than related to the prebiotic effect of the sugars. So, in order to gain more insight into the putative effects of lactulose and inulin on the cecal bacterial flora of piglets, we conducted the following piglet study. Because clostridia species have been thought to be major sources for colonic butyrate production,13,14 we nominally hypothesized that feeding piglets with supplementary lactulose or inulin would increase cecal densities of clostridia. |
| Databáze: | OpenAIRE |
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