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Activation of GLP-1R suppresses food intake and induces postsynaptic depolarization of membrane potential (Figure 1A) and/or presynaptic modulation of glutamatergic or GABAergic neurotransmission (Figure 1B)

This article breaks down that paradox, explains why discomfort is such a powerful biological signal, and shows how intensity shapes everything from lactate metabolism to brain chemistry to long-term resilience

To learn more, please see a recent article from The New York Times that featured our study findings

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Elevated cortisol levels (your bodys main stress hormone) can blunt GLP-1 production and disrupt appetite signals

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