Developmental aspects of gastric inhibitory polypeptide (GIP) and its possible role in the enteroinsular axis in neonates.
Little is known on the development of the release of gastric inhibitory polypeptide (GIP) in neonates or on its potential role in the enteroinsular axis. Using cross-section data collection we studied: (a) 100 preterm neonates either at birth (cord blood), or before or after a feed on the sixth or 24th day and (b) 63 term neonates at birth or on the sixth day. Blood samples were assayed for GIP, insulin and glucose. At birth plasma GIP concentrations were low compared with fasting adults (p less than 0.01). Basal plasma levels were significantly higher at six days in fed infants, but not in a group of sick preterm infants who had never been fed orally. On the sixth day there was no GIP response to a feed, but by 24th day there was a marked postprandial elevation (p less than 0.01). In preterm infants the insulin response was 68% greater at 24 days than at six days in spite of a similar glycaemic response. We hypothesize that this increasing postnatal insulin response to enteral feeding may be due to the commencement of the postprandial release of GIP, thought to be an important effector in the enteroinsular axis.
D001786:Blood Glucose / Q000032:analysis; D005260:Female; D005749:Gastric Inhibitory Polypeptide / Q000378:metabolism*; D005768:Gastrointestinal Hormones / Q000378:metabolism*; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D007328:Insulin / Q000097:blood; D008297:Male; D008895:Milk, Human
D001786:Blood Glucose; D005768:Gastrointestinal Hormones; D007328:Insulin; D005749:Gastric Inhibitory Polypeptide