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.
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.
Abstract:
Release of endogenous cholecystokinin (CCK) from the small intestine by gastric loads was investigated in rats on postnatal days 9--12 (P9--P12). After 5--6 h of deprivation, pups received 5% b.wt. loads of water, 0.9% NaCl, 20% glucose, 20% maltose, 200 mg soybean trypsin inhibitor (SBTI) in 0.9% saline or sham load. Plasma was collected 15 min after the loads, and the concentration of bioactive CCK was measured by a specific and sensitive bioassay. Loads of SBTI and water significantly increased plasma CCK compared to sham loads, but loads of saline, glucose, and maltose did not. The efficacy of the water load was not demonstrated in adult rats. The results suggest that the previously reported reduction of intake during independent ingestion by hypertonic preloads of glucose and maltose was not mediated by the release of CCK sufficient to be detected in the plasma under these conditions.
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