ABSTRACT
Lipolytic activity was studied in aspirates from the esophageal pouch and from the stomach of eight infants with congenital esophageal atresia. Lipolytic activity, tested with doubly labeled ([3H]glyceryl, [14C]fatty acid) long-chain triglyceride was present in esophageal and gastric aspirates. The activity in esophageal aspirates was in the range of 2.7-130 nmol/min/ml aspirate and that in gastric aspirates was in the range of 2.9-40.4 nmol/min/ml aspirate. The reaction products of lipolytic activity in esophageal and gastric aspirates were a mixture of mono- and diglycerides, glycerol, and free fatty acids. The lipolytic activity at the two sites--esophagus and stomach--varied with respect to pH optimum (5.0-7.6 and 6.0-6.5, respectively) and reaction products (glycerol 41.6 +/- 20% and 7.3 +/- 4.6%, respectively). These findings confirm the earlier observations that digestion of dietary fat is initiated in the stomach and suggest that the lipolytic activity present in gastric contents originates concomitantly from the oral-esophageal area as well as from the stomach. These studies do not exclude the possibility that the lipolytic activity in the stomach of infants with esophageal atresia could originate in regurgitated intestinal contents.
Subject(s)
Esophageal Atresia/enzymology , Esophagus/enzymology , Lipase/metabolism , Stomach/enzymology , Female , Humans , Infant, Newborn , Lipolysis , Male , Triglycerides/metabolismABSTRACT
The possible compensatory role of human milk lipase in the digestion of dietary fat was examined in a group of very low-birth-weight infants. Fat excretion was studied in 15 preterm infants of gestational age 26 to 33 weeks and birth weight 660 to 1,695 gm. The amount and composition of fecal fat were determined in stools collected for 72 hours. Eight infants were fed Similac 24 LBW exclusively and seven infants were fed a mixture of fresh human milk (40%) and formula (60%). Fat excretion was lower in infants fed a mixture of human milk and formula than in infants fed formula only (4.7% -+/- 0.50% vs 11.9% +/- 1.4% of intake, respectively). Excretion of calcium soaps, when expressed as percent of total fat, was higher in the group fed the human milk-containing diet (18.9% +/- 13.5%), than in the group fed formula only (6.8 +/- 2.5%); however, the absolute amounts excreted were similar in both groups (65 +/- 46 and 45 +/- 17 mg/kg/day, respectively). The lower fat excretion in infants fed a mixture of fresh human milk and formula could be related to the lipase present in human milk. These data suggest that human milk lipase probably contributes to the digestion and absorption of dietary fat in the "tiny premature" infant.
Subject(s)
Dietary Fats/metabolism , Digestion , Infant Food , Infant, Low Birth Weight , Milk, Human/metabolism , Feces/analysis , Female , Humans , Infant, Newborn , Intestinal Absorption , Lipase/metabolism , Lipids/analysis , Male , Milk, Human/enzymologyABSTRACT
Lipolytic activity was studied in gastric aspirates of 13 premature infants of birth weight 1,050 to 1,786 gm. All infants received a diet of infant formula fed by gastric tube. Gastric aspirates were collected after irrigating the stomach with 2 to 5 ml sterile saline before regular feeding. Lipolytic activity, tested with doubly labeled 3H glyceryl-14 C tripalmitin substrate, was 55.6 +/- 11.7 n mol/min/ml (range 4.2 to 140). The lipolytic activity had a pH optimum of 5.4 and produced partial glycerides (mono and diglycerides), glycerol, and free fatty acids. Lipolysis was inhibited by bile salts. Our findings show that in premature infants, as in adults, digestion of dietary fat starts in the stomach. Since bile salt concentrations are low in premature infants, the amphiphilic reaction products formed (monoglyceride and FFA) could play a significant role in the stabilization of lipid emulsions.
