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Updated: Dec 4, 2025

Mechanisms Underlying Gut Hormone Secretion Using the Isolated Perfused Rat Small Intestine
Published on: February 26, 2019
Effects of passage through the digestive tract on incretin secretion: Before and after birth
Seiichi Tomotaki1, Ryosuke Araki1, Kouji Motokura1
1Department of Pediatrics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Insights
Fetal incretin secretion is not stimulated by amniotic fluid passage. Postnatal enteral feeding is crucial for incretin hormone release in infants.
Area of Science:
- Neonatal physiology
- Endocrinology
- Gastroenterology
Background:
- Endogenous incretins, such as glucagon-like peptide-1 (GLP-1) and gastric inhibitory peptide/glucose-dependent insulinotropic polypeptide (GIP), are secreted by the fetus.
- The specific stimuli for fetal incretin secretion remain unclear.
- Investigating the role of amniotic fluid passage through the fetal intestine is essential to understand these stimuli.
Purpose of the Study:
- To determine if the passage of amniotic fluid through the intestinal tract stimulates fetal incretin secretion.
- To compare fetal incretin levels in infants with and without duodenal atresia.
- To examine the relationship between postnatal enteral feeding and incretin secretion.
Main Methods:
- Umbilical cord blood samples were collected from infants with duodenal atresia and normal controls (term and preterm).
- Concentrations of GLP-1 and GIP were measured in umbilical cord blood.
- Postnatal blood samples were analyzed for incretin levels in relation to enteral feeding amounts.
Main Results:
- Umbilical vein GLP-1 and GIP levels were comparable between infants with duodenal atresia and normal infants.
- Positive correlations were observed between the volume of enteral feeding and postnatal serum concentrations of GLP-1 (r=0.47) and GIP (r=0.49).
Conclusions:
- Enteral feeding significantly stimulates GLP-1 and GIP secretion in postnatal infants.
- Amniotic fluid passage through the digestive tract does not appear to be a significant factor in fetal incretin secretion.
- The mechanisms regulating incretin secretion likely differ between the fetal and postnatal periods, with other unidentified factors stimulating fetal secretion.
Aims/Introduction:
It was reported that fetuses secrete endogenous incretin; however, the stimulants of fetal incretin secretion are not fully understood. To investigate the association between the passage of amniotic fluid through the intestinal tract and fetal secretion of incretin, we analyzed umbilical cord incretin levels of infants with duodenum atresia.
Materials And Methods:
Infants born from July 2017 to July 2019 (infants with duodenum atresia and normal term or preterm infants) were enrolled. We measured and compared the concentrations of glucagon-like peptide-1 (GLP-1) and gastric inhibitory peptide/glucose-dependent insulinotropic polypeptide (GIP) in the umbilical vein and preprandial blood samples after birth.
Results:
A total of 98 infants (47 term, 46 preterm and 5 with duodenum atresia) were included. In patients with duodenum atresia, umbilical vein GLP-1 and GIP levels were the same as those in normal infants. In postnatal samples, there were positive correlations between the amount of enteral feeding and preprandial serum concentrations of GLP-1 (r = 0.47) or GIP (r = 0.49).
Conclusions:
Our results show that enteral feeding is important for secretion of GLP-1 and GIP in postnatal infants, whereas the passage of amniotic fluid is not important for fetal secretion of GLP-1 and GIP. The effect of ingested material passing through the digestive tract on incretin secretion might change before and after birth. Other factors might stimulate secretion of GLP-1 and GIP during the fetal period.
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