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These findings position the entero-gustatory-endocrine axis as a therapeutic target in metabolic disorders, where GLP-1 dysfunction disrupts taste signaling, perpetuating pathological feeding behaviors ( Figure 3 )

While these changes are therapeutic in patients being treated, their impact on plasma composition in a donor setting remains unstudied

Given our previous findings of mTOR upregulation in LMNA (A539V), inhibiting mTOR with rapamycin in LMNA (A539V) fish may potentially rescue muscle strength

Specifically, projections from GLP1R-expressing neurons in the AP and NTS to hypothalamic nuclei involved in energy homeostasis drive food intake inhibition

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The combination of variants linked to a slightly increased risk of liver damage could add together to increase the risk more significantly