Comparison of methods for estimating fecal carbohydrate excretion in premature infants.

Our previous studies have suggested that there is minimal fecal excretion of carbohydrate-derived energy in premature infants fed lactose or glucose-polymer as the source of carbohydrate. In these studies, carbohydrate energy excretion was equated with the non-nitrogenous, nonfat energy. Although these studies provided consistent results, this methodological approach cannot distinguish actual excretion of dietary carbohydrate from carbohydrate in the form of large molecular compounds derived from infant or bacterial cells (which in fact comprise approximately 90% of the measured value). Therefore, in this study we compared the absorption of carbohydrate energy to the fractional absorption of 13C derived from [D-1-13C]-lactose in 10 premature infants 30-32 weeks gestational age fed either a commercial premature infant formula containing a mixture of carbohydrates (50% lactose: 50% glucose polymer) or the same formula in which lactose was the sole carbohydrate. The two methods provided comparable estimates of carbohydrate absorption (96 and 94%, respectively), although there were significant discrepancies in two infants. These studies provide evidence of external validity for the two methods.

Efficient assimilation of lactose carbon in premature infants.

Previous studies have shown that there is minimal fecal excretion of carbohydrate energy in premature infants with high breath H2 concentrations, implying that the colon plays an important role in salvaging lactose energy. The present study extends this work by using a stable isotope method for serial assessment of lactose carbon excretion. Thus, in nine premature infants (30-32 weeks of gestation and 11-36 days of age), we conducted 23 longitudinal studies of breath hydrogen concentration and the cumulative fecal excretion of 13C derived from a single dose of [D-1-13C]lactose. The ranges of values (mean +/- SD) for breath hydrogen concentration and lactose absorption were respectively 4-440 ppm/5% CO2 (92 +/- 100) and 82-100% tracer dose (98.4 +/- 3.9). In 21 studies, lactose carbon excretion was less than 2% of the dose. There was a significant correlation between postnatal age and breath hydrogen concentration (R = 0.48; p = 0.02). These studies suggest that colonic fermentation activity is adequate for efficient colonic salvage of lactose even during the second week of life.

Stable isotope model for estimating colonic acetate production in premature infants.

In premature infants, a nutritionally significant proportion of lactose is apparently fermented in the colon to acetate. To estimate the rate of entry of acetate into the peripheral circulation, a model that takes into account extraction of gut-derived acetate by splanchnic and hepatic tissues was developed. Using a [1-13C]acetate orogastric infusion technique, six studies were carried out on five premature infants during constant orogastric feeding. Ranges in gestational age, postnatal age, and breath H2 concentration (corrected for CO2 content) were 28-32 weeks, 16-29 days, and 45-252 microL/L, respectively. The estimated rate of entry of acetic acid (mean +/- SD) was 63.7 +/- 33.8 mumol.kg-1.min-1 (range, 22.9-123.2 mumol.kg-1.min-1), which corresponded to 64.3% +/- 38.6% (24%-136%) of the potential two carbon units from dietary lactose. Thus, a substantial fraction of dietary lactose in premature infants may be converted to acetic acid; this conversion could have a significant effect on protein as well as energy requirements.