Abstract 653

In preterm infants or patients with short bowel syndrome, fermentation of carbohydrate in the colon can be a significant source of metabolizable energy. However, based on in vitro, fecal fermentation studies, it has been suggested that disaccharide fermentation can not serve as a source of butyric acid( J Nutr 118:321). Thus, one might speculate that fermentation of sugars in formula diets may not prevent colitis associated with sugar malabsorption (J Pediatr 118:321) by producing butyric acid (Gastroent 103:51). As part of an effort to determine if butyric acid deficiency contributes to colitis during sugar malabsorption (FASEB J 12:A736), we modified our technique for assessing in vivo production of short chain fatty acids in the colon (J Nutr 126:3069) based on the assumption that endogenous production of butyric acid was minimal and consistent. In 7 non-fasting, acutely anesthetized piglets (aged 24-30 d), we conducted 120 min cecal infusions of [1-13C]-butyric acid and unlabeled sugar (42 mg/min)(lactose, N=5)(lactulose, N=2) and estimated the rate of production of butyric acid (Ra BA) from the ratio of the rate of tracer infusion to the fractional molar enrichment of butyric acid in the artery. Ra BA (mean ±SEM)(µmol/kg/min) was respectively 2.8± 0.4 and 5.0 ± 0.4 for the lactose and lactulose studies equating to a mean of 18.6% and 29.4% of the unlabeled sugar infusion. Thus, butyric acid may be an important by-product of colonic fermentation of disaccharide in the piglet.

Funded by: CHRF; Ross Product Division of Abbott Laboratories; CCFA