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* Department of Pediatrics, The Ohio State University College of Medicine and Children's Hospital, Columbus, OH 43205
Department of Nutrition, Case Western Reserve University and Mt. Sinai Hospital, Cleveland, OH 44106
Sugar reaching the colon because of intestinal maldigestion or malabsorption may be fermented to acetate and other short-chain fatty acids, resulting in stimulation of colonic water absorption and cell proliferation. To explore this phenomenon in more detail, we have developed a stable isotope model for estimating the fraction of colon-derived glucose or lactose that is fermented to acetate, propionate and buty-rate. In an initial application of the model, [d3]-acetate and either [1-13C]-glucose or [D-1-13C]-lactose were infused into the cecum or colon of piglets, and plateau plasma acetate enrichment was monitored in the carotid artery. In acutely anesthetized piglets, the fractions of glucose and lactose fermented to acetate were 17.0 and 20.0%, respectively. In a chronically catheterized piglet, fermentation was higher (34.2%). When conducted in chronically catheterized animals or via a colostomy or ileostomy in infants, this model may be used to determine how age, previous surgery or antibiotic therapy affects the efficiency of colonic assimilation of carbohydrate.
KEY WORDS: acetate short-chain fatty acid fermentation of sugar stable isotopes pigs
1 Supported by National Institutes of Health grant HD 19773.
2 The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.
3 To whom correspondence and reprint requests should be addressed.
Manuscript received 23 February 1996. Revision accepted 4 September 1996.
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