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Enterostatin: a gut-brain peptide regulating fat intake in rat
M Sörhede1, J Mei, C Erlanson-Albertsson
1Department of Medical and Physiological Chemistry 4, University of Lund, Sweden.
Journal of Physiology, Paris
|January 1, 1993
Summary
Enterostatin (VPGPR) significantly inhibits high-fat food intake at a low dose but loses this effect at higher doses. This suggests complex interactions with brain receptors influencing fat consumption.
Area of Science:
- Neuroscience
- Physiology
- Pharmacology
Background:
- Enterostatin, a peptide fragment of procholecystokinin, is implicated in regulating food intake.
- The precise mechanisms by which enterostatin influences macronutrient selection, particularly fat intake, remain incompletely understood.
Purpose of the Study:
- To investigate the dose-dependent effects of enterostatin on high-fat food intake in rats.
- To explore the binding characteristics of enterostatin in rat brain membranes.
Main Methods:
- Intravenous administration of enterostatin (38 nmol and 76 nmol) to food-deprived rats.
- Measurement of high-fat food intake following enterostatin injection.
- In vitro binding assays using tritiated enterostatin and crude rat brain membranes.
Main Results:
- A dose of 38 nmol enterostatin significantly inhibited high-fat food intake.
- The inhibitory effect was abolished at a higher dose of 76 nmol, with a slight increase in intake observed initially.
- Binding studies revealed two affinity sites for enterostatin in brain membranes (Kd = 0.5 nM and Kd = 170 nM).
Conclusions:
- Enterostatin exhibits a biphasic effect on high-fat food intake, inhibiting at low doses and potentially stimulating at high doses.
- The presence of high- and low-affinity binding sites suggests interaction with distinct receptor subtypes.
- These findings provide insights into the complex neurobiological regulation of fat appetite by enterostatin.