Effect of human milk or formula on gastric function and fat digestion in the premature infant.

The effect of diet, human milk or formula, on gastric function (lipase and pepsin activity, pH, and volume) and intragastric digestion of fat was assessed in 28 appropriate for gestational age preterm infants (gestational age, 28.9 +/- 1.4, 29.1 +/- 0.9, 29.5 +/- 0.6 wk; birth weight, 1.00 +/- 0.14 to 1.18 +/- 0.07 kg). The infants were fed either human milk (n = 11), SMA Super Preemie formula (n = 9), or Similac, Special Care formula (n = 8). Fasting and postprandial activity of digestive enzymes, pH, and gastric volume (measured before or during 50 min after gavage feeding) did not differ as a function of diet among the three groups of infants. Gastric lipase output, 23.1 +/- 5.1, 28.3 +/- 6.6, and 22.5 +/- 6.4 (U/kg of body weight) in human milk-, SMA SP-, or Similac SC-fed infants was comparable to the gastric lipase output of healthy adults fed a high fat diet (22.6 +/- 3.0). Pepsin output was, however, significantly lower (597 +/- 77, 743 +/- 97, and 639 +/- 142 U/kg of body weight) in human milk-, SMA SP-, and Similac SC-fed infants) than in healthy adults (3352 +/- 753 U/kg). The hydrolysis of dietary fat was 1.7-2.5-fold higher (p < 0.01) in human milk-fed infants than in infants fed either formula. We conclude that differences in type of feeding, i.e. different fatty acid profiles (long chain or medium chain triglycerides), different emulsions (natural or artificial), and different fat particle sizes do not affect the level of activity of gastric enzymes. However, the triglyceride within milk fat globules appears to be more accessible to gastric lipase than that within formula fat particles. We suggest that the contribution of gastric lipase to overall fat digestion might be greater in the newborn (a period of pancreatic insufficiency) than in the adult.

Dietary fat modulates gastric lipase activity in healthy humans.

The aim of this study was to determine whether the amount of dietary fat modulates the activity of gastric lipase in humans. Gastric juice was collected from six healthy subjects after 2-wk periods of either a high-fat (50% of energy as fat) or low-fat (25% of energy as fat) diet. The collection period lasted 2 h, the first hour under baseline conditions and the second hour after pentagastrin stimulation (6 micrograms/kg body wt). Gastric lipase and pepsin activities were quantitated at 15-min intervals and total enzyme outputs were calculated. Under baseline conditions there was a tendency for higher output of gastric lipase and pepsin after the high-fat diet than after the low-fat diet (gastric lipase: 745 compared with 446 U/h, pepsin: 107,677 compared with 78,505 U/h). The difference in output between diet groups was significant after pentagastrin stimulation (gastric lipase: 1323 compared with 875 U/h, pepsin: 191,751 compared with 128,961 U/h, for high-fat compared with low-fat diet, respectively, P < 0.05). This study is the first to report that a high-fat diet leads to an increase in the activity of gastric enzymes in humans.