Inhibitory effects of peripheral administration of exendin-4 on food intake are attenuated by lesions of the central nucleus of amygdala.
Brain Res Bull · 2019
Last updated 2026-05-28In a study on rats, a drug called exendin-4 (a GLP-1 receptor agonist) reduced intake of high-sucrose food but not regular chow. When the central nucleus of the amygdala (CeA) was damaged, the drug’s ability to reduce high-sucrose food intake was weakened, suggesting the CeA plays a role in this effect.
AI summary of the abstract below.
| Journal | Brain Res Bull, 2019 |
|---|---|
| Citations | 6 |
| Relative citation ratio | 0.25 |
| NIH percentile | 16 |
| Molecules | — |
| Conditions studied | Obesity |
Abstract
The long-acting glucagon-like peptide-1 receptor (GLP-1R) agonist exendin-4 suppresses food intake and decreases body weight. However, the mediating site(s) of action of the anorectic effects induced by peripheral administration of GLP-1R agonists are not well known. The present study investigated the effects of bilateral lesions of the central nucleus of the amygdala (CeA) on the suppression of chow and high-sucrose food intake by exendin-4 in rats. Adult male Sprague-Dawley rats with bilateral sham or electrolytic lesions (400 μA; 25 s) of the CeA were used for this experiment. No significant difference was found in the daily chow intake and high-sucrose food intake in rats with CeA lesion compared to sham-operated rats. Bilateral lesions of the CeA significantly attenuated the suppression of high-sucrose food intake by i.p. exendin-4, but not the suppression of chow intake. These results suggest that a mediating role of the CeA on the peripheral effects of exendin-4.
Verbatim abstract via PubMed 30862486 ↗