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Based on these observations with GEP12, and on our unexpected findings that GEP44-mediated increases in ISR and decreases in glucagon release can be detected only in the presence of Y1-R antagonists, we proceeded to characterize the contributions of Y1-R to glucose uptake in muscle tissue

These mechanisms indicate that decrements in GLP-1R efficacy are not merely the result of receptor downregulation but are rooted in a fundamental disruption of the intracellular environment, driven by organelle stress and lipotoxic signaling

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doi: 10.1006/abbi.1996.0482