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doi: 10.1007/s00253-024-13367-0 22 KoshiD.UeshimaH.KawauchiM.NakazawaT.SakamotoM.HirataM.et al

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While studies explore plausible mechanisms (NO-system modulation, VEGFR2-Akt-eNOS signaling, GHR/JAK2 in tendon cells), well-controlled human trials are limited

The mechanism enhanced phosphatidylcholine synthesis and improved VLDL export directly targets the hepatic lipid accumulation that defines fatty liver

The weight loss and metabolic improvements from cagrilintide produce downstream effects on multiple cardiovascular risk factors