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Where estrogen works to restore the hormonal environment that governs fat distribution and metabolic regulation, GLP-1 therapy directly reduces caloric intake by recalibrating appetite signaling, improves glycemic control through multiple mechanisms, and drives the reduction of visceral fat mass that estrogen alone cannot reliably produce in the setting of significant metabolic burden

These findings indicate that D1R-dependent repression of novel-m009C relieves inhibition of Grin1, enhancing NMDAR signaling to promote METH reward 109

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