By directly reducing circulating glucose and free fatty acid levels, and potentially enhancing hepatic fatty acid oxidation through GCGR agonism, these agents may deprive tumor cells of essential nutrients, thereby interfering with metabolic reprogramming processes (55,65,69,70)
Engel, S
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2 Mechanism of atrial fibrillation To date, the pathogenesis of AF remains incompletely understood and is believed to primarily involve the following aspects: Myocardial metabolic dysfunction: (1) During AF, myocardial metabolism undergoes marked alterations, characterized by reduced efficiency of fatty acid oxidation
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