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Central leptin modulates behavioral and neural responsivity to CCK
M Emond1, G J Schwartz, E E Ladenheim
1Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
The American Journal of Physiology
|May 8, 1999
Summary
Leptin enhances satiety signals from CCK, influencing food intake. This study reveals leptin
Area of Science:
- Neuroscience
- Endocrinology
- Physiology
Background:
- Leptin, a hormone regulating appetite, has unclear mechanisms influencing food intake.
- Within-meal satiety signals are crucial for controlling meal size.
Purpose of the Study:
- To investigate if leptin modulates the satiety effects of cholecystokinin (CCK).
- To explore the neural pathways involved in leptin-CCK interactions on food intake.
Main Methods:
- Administration of leptin and CCK to rats via third ventricular injection.
- Measurement of liquid diet intake.
- Analysis of c-Fos activation in brain regions (area postrema, nucleus of the solitary tract, paraventricular nucleus).
Main Results:
- Leptin alone did not affect food intake but dose-dependently enhanced CCK-induced satiety.
- Combined leptin and CCK increased c-Fos activation in the area postrema and nucleus of the solitary tract.
- Leptin-CCK treatment elevated c-Fos activation in the paraventricular nucleus compared to leptin alone.
Conclusions:
- Leptin's effects on food intake are mediated by modulating responses to within-meal satiety signals.
- Leptin interacts with CCK signaling in key brainstem and hypothalamic areas to regulate appetite.