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Our findings revealed that Y1-R signaling directly stimulated glucose uptake in muscle tissue via a pathway that is independent of insulin-stimulation

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Similar to HNF4 knockdown, knocking individual SAA enzymes led to various degrees of resistance to methionine/cystine restriction or sorafenib treatment (Fig

DOX treatment significantly increased the apoptotic DNA fragmentation index in skeletal muscle by approximately 100% compared to controls, confirming its pro-apoptotic toxicity