Release of endogenous cholecystokinin in response to gastric preloads in rats on postnatal days 9--12

A Weller1, I H Gispan, R C Ritter

  • 1Developmental Psychobiology Laboratory, Department of Psychology, Bar Ilan University, Ramat Gan S2900, Israel.

Physiology & Behavior
|March 10, 2001
PubMed

Insights

Soybean trypsin inhibitor and water loads increased cholecystokinin (CCK) in infant rats. Hypertonic glucose or maltose loads did not release significant CCK, suggesting CCK is not the primary mediator of reduced intake in young rats.

Area of Science:

  • Physiology
  • Gastroenterology
  • Developmental Biology

Background:

  • Endogenous cholecystokinin (CCK) plays a role in regulating gastrointestinal functions, including satiety.
  • Gastric loads are known to stimulate CCK release from the small intestine.
  • The role of CCK in early postnatal development and its response to different gastric stimuli requires further investigation.

Purpose of the Study:

  • To investigate the release of endogenous CCK in response to various gastric loads in infant rats.
  • To determine if CCK release is mediated by specific nutrients or osmotic load in early development.
  • To assess the contribution of CCK to intake regulation during early postnatal life.

Main Methods:

  • Infant rats (postnatal days 9-12) were deprived of food for 5-6 hours.
  • Gastric loads included water, saline, glucose, maltose, or soybean trypsin inhibitor (SBTI).
  • Plasma CCK concentrations were measured 15 minutes post-load using a specific bioassay.

Main Results:

  • Gastric loads of SBTI and water significantly increased plasma CCK levels compared to sham loads.
  • Saline, glucose, and maltose loads did not significantly alter plasma CCK concentrations.
  • The effect of water load on CCK release was not observed in adult rats.

Conclusions:

  • Infant rats exhibit CCK release in response to specific stimuli like SBTI and water.
  • Hypertonic glucose and maltose loads do not appear to trigger significant CCK release in infant rats.
  • CCK is unlikely to be the primary mediator for intake reduction observed with hypertonic preloads in early development.

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