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The study showed that the drug interacted with the GLP-1 receptor to a much higher degree than with the glucagon receptor, indicating that any pharmacological effects were likely mediated via GLP-1R activation
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The inhibition, which shows dose dependency, is exerted via interactions with receptors in the brain that are accessible via leaks in the blood-brain barrier of the circumventricular organs, mainly the postrema area, the subfornical organ and the median eminence [10, 11]
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