gastrins and Food-Hypersensitivity

The biologic clock that determines the temporal sequence of maturation of digestive and absorptive processes in the gastrointestinal tract is genetically predetermined, but may be modified by dietary, hormonal, or other factors. In general it may be said that the gastrointestinal tract of full-term neonates is capable of digesting and absorbing a nutritionally adequate quantity of dietary protein but capacity is limited. Very low birth weight preterm infants, who are surviving the early neonatal period in increasing numbers, have immaturity of a wide range of digestive and membrane-associated absorptive processes; in addition macromolecular absorption may be increased. Whether a limited capacity to digest food protein results in increased or altered antigenic stimulation of these immature infants remains speculative with present knowledge. Immaturity of intestinal lactase may lead to problems of lactose intolerance, but there is recent evidence that lactase activity may be inducible by milk feeding.

Topics: Absorption; Aging; Amino Acids; beta-Galactosidase; Biological Transport, Active; Cholecystokinin; Dietary Proteins; Digestion; Digestive System; Endopeptidases; Exopeptidases; Fetus; Food Hypersensitivity; Gastric Acid; Gastrins; Humans; Hydrolysis; Infant; Infant, Newborn; Infant, Premature; Intestinal Mucosa; Lactose Intolerance; Pancreas; Pepsin A; Peptide Hydrolases; Secretin; Stomach; Substrate Specificity

Priming of the gastrointestinal (GI) tract with low-volume feedings before giving full enteral feedings to very premature, high-risk infants is a controversial practice. We designed a study of infants weighing less than 1,250 g and receiving total parenteral nutrition to determine whether GI priming would hasten weight gain, improve tolerance of subsequent feedings, enhance nutritional status, and increase serum concentration of gastrin, a hormone trophic for intestinal growth. Infants were randomly assigned to receive total parenteral nutrition (TPN) alone (N = 21) or GI priming plus TPN (N = 19) for 12 days beginning on day 3 of life. Full-strength premature infant formula was used for priming. Both groups received the same total nutrition. Beginning on day 15, feedings in both groups were increased daily to a maximum of 120 kcal/kg/day on day 20, where they were maintained until day 30. After day 30, the feedings were modified according to the infants' condition. The groups did not differ in birth weight, gestational age, or 5-min Apgar scores. GI-primed infants had improved feeding tolerance after day 20 and a faster rise in serum gastrin during the initial phase of the study. There was no significant difference in weight gain. GI priming improves tolerance of feedings, accelerates rate of rise of serum gastrin during the first weeks of life, and does not increase the risk of feeding complications when compared to TPN alone. This may lead to more rapid maturation of the GI tract in primed infants.

Topics: Eating; Enterocolitis, Pseudomembranous; Female; Food Hypersensitivity; Gastrins; Humans; Infant, Low Birth Weight; Infant, Newborn; Infant, Premature; Male; Parenteral Nutrition, Total; Prospective Studies; Random Allocation; Weight Gain

The assessment of the serum gastrin concentrations and the role of enterohormone in children with primary acid gastroesophageal reflux (GER) and GER secondary to cow's milk allergy (CMA).. 138 children were diagnosed with pathological acid GER on the basis of pH-metric examination. 76 (28.8%) patients had primary GER and 62 (23.5%) patients had GER secondary to CMA.Serum gastrin concentration (fasting and postprandial) was assessed before treatment and 1 and 2 years after initiation of the therapy.. The children with primary GER had the fasting gastrin concentration 69.46 ± 11.87 μU/ml before treatment, 77.86 ± 26.35 μU/ml after 1 year and 83.78 ± 25.21 μU/ml after 2 years of treatment. The children with GER secondary to CMA had gastrin concentrations 89.61 ± 26.75, 73.17 ± 19.49 and 73.90 ± 20.31 μU/ml respectively. The mean postprandial gastrin concentration after treatment was higher than before treatment in children with both primary and secondary GER. The primary GER group had postprandial gastrin concentration 96.07 ± 33.51 μU/ml before treatment and 116.06 ± 33.95 μU/ml and 118.48 ± 33.96 μU/ml after 1st and 2nd year of therapy respectively. The secondary GER group had postprandial gastrin concentration 85.33 ± 14.12 μU/ml before treatment and 106.55 ± 24.51 μU/ml and 110.36 ± 24.67 μU/ml after 1st and 2nd year of therapy respectively.. The mean fasting serum gastrin concentrations in patients with primary and secondary GER were similar and mean postprandial concentrations were higher than fasting concentrations in both study groups.

Topics: Animals; Cattle; Child, Preschool; Esophageal pH Monitoring; Female; Food Hypersensitivity; Gastric Acidity Determination; Gastrins; Gastroesophageal Reflux; Humans; Hydrogen-Ion Concentration; Infant; Male; Milk; Milk Hypersensitivity; Postprandial Period; Time Factors

Topics: Adolescent; Asthma; Biopsy; Child; Child, Preschool; Dermatitis, Atopic; Female; Ferritins; Food Hypersensitivity; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Humans; Infant; Intestinal Mucosa; Jejunum; Male; Rhinitis, Allergic, Perennial

The effect of fat and protein meals on the lower oesophageal sphincter pressure was tested in normal subjects using an infused open-tipped manometric system. After ingestion of a minced beef meal, the mean peak pressure at the lower oesophageal sphincter increased 5.8 +/- 1.5 mm Hg (+/- 1 SE). By contrast, ingestion of a corn oil meal resulted in a mean peak decrease of 7.8 +/- 1.9 mm Hg. Following the combined minced beef/corn oil meal, mean peak pressure decreased 3.0 +/- 2.1 mm Hg. Pentagastrin (3 mug/kg, subcutaneously) resulted in a mean peak increase of 20.6 +/- 7.0 mm Hg when given to the subjects in the fasting state, and produced an increase of only 8.4 +/- 1.7 mm Hg when given following the fat meal. Finally, after a mean peak decrease in pressure at the lower oesophageal sphincter of 6.8 +/- 1.0 mm Hg 15 minutes after the corn oil meal, gastric alkalinization with 30 ml of antacid resulted in a subsequent increase in sphincter pressure of 5.2 +/- 1.6 mm Hg. These data indicate: (1) Fat attenuates the effect of endogenous gastrin as well as exogenous pentagastrin stimulation of the lower oesophageal sphincter. (2) Fat-induced incompetency of the lower oesophageal sphincter can be effectively combated by gastric alkalinization in the form of antacids.

Topics: Adult; Antacids; Dietary Fats; Dietary Proteins; Esophagogastric Junction; Fasting; Fats; Food Hypersensitivity; Gastrins; Humans; Male; Meat; Oils; Pentagastrin; Pressure; Zea mays