Prolactin and oxytocin as modulators of intestinal contractility and glucose uptake

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Authors: Perla Alejandra Figueroa-Carrasco, Aída Jimena Velarde-Salcedo, Carmen Gonzalez
Cited by: 1
References: 72

Abstract

Introduction: Prolactin (PRL) and oxytocin (OT) are bioactive hormones naturally present in maternal milk that support neonatal development, contribute to immune regulation and gut maturation in infants, and promote growth and cell differentiation in the small intestine. However, the individual and combined roles of these hormones in intestinal function remain unclear. This study aims to elucidate the physiological effects of PRL and OT on intestinal motility, nitric oxide (NO) production, and glucose uptake to better understand their influence during early development. Methods: Precontracted intestinal segments were placed in physiological solution, connected to isometric transducers, and exposed to various concentrations of PRL, OT, or PRL + OT, and changes in contractile responses were recorded. Glucose uptake was measured using everted sacs, and NO production was measured via the Griess method. PRL, OT, and PRL + OT modulated intestinal contractile activity, with effects varying by segment. OT induced higher NO levels than PRL at cumulative concentrations. Results and discussion: A single concentration of PRL or OT mostly preserved the contraction vs. % of the maximal contraction induced by KCl (100%), while PRL + OT reduced it and NO production in the duodenum and jejunum, but not in the ileum. Individually, PRL and OT increased glucose uptake, while their combination inhibited it, suggesting a modulatory mechanism regulating nutrient absorption. These findings support the role of PRL and OT as maternal milk-derived regulators of intestinal functions.

Fields of Study & Subjects

Neuroendocrine regulation and behavior Infant Nutrition and Health Breastfeeding Practices and Influences

Publication details

Journal / source
Frontiers in Physiology
Publisher
Frontiers Media SA
Volume
17
Pages
1703887–1703887
Publication date
26 February 2026
Language
EN