Research

Hormonal

Intracerebroventricular administration of the GLP-1 receptor agonist Exendin-4(1-32)K-capric acid (Ex-4c) suppresses food intake and body weight gain in mice by directly activating arcuate pro-opiomelanocortin (POMC) neurons.

This research identifies that a specific GLP-1 agonist (Ex-4c) reduces food intake by directly activating POMC neurons in the hypothalamus. The mechanism involves the closure of KATP channels via PKA-dependent signaling. While this is preclinical data in mice, it supports the broader class of GLP-1 agonists used for obesity treatment by confirming a central neural mechanism involving appetite suppression.

GoodSupportsHIGH confidence
Our findings indicate that the appetite-suppressing effects of Ex-4c depend on pro-opiomelanocortin (POMC) neurons... Ex-4c activated POMC neurons in the arcuate nucleus of the hypothalamus.
Sujin Yoo et al. · Endocrinology and Metabolism · 2025

Why this rating

High-quality mechanistic evidence using multiple methods (patch-clamp, immunohistochemistry, ablation) in a controlled animal model, though not human clinical data.

Source

Exendin-4(1-32)K-Capric Acid, a Glucagon-Like Peptide-1 Receptor Agonist, Suppresses Food Intake via Arcuate Pro-Opiomelanocortin Neurons

Sujin Yoo et al. · Endocrinology and Metabolism · 2025

DOI 10.3803/enm.2024.2185

mechanism_onlyCited 3×
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DOI resolved against Crossref · corpus check 2026-06-10

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