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Molecular hypothalamic profiling revealed common and distinct proteins and pathways being affected by GLP1/E in the two PCOS models, with a consistently higher number of individual proteins being differentially expressed (DE), either up- or down-regulated, in the hypothalamus of PWA mice treated with GLP1/E vs

HGF activates c-MET receptor in a paracrine manner by exerting its pleotropic effects through controlling several transmission cascades such as the mitogen-activated protein kinase (MAPK), phosphatidylinositol-3 kinase (PI3K)/AKT, and Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathways [7]

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The journey from high-risk HLA alleles and viral mimicry to targeted destruction of pancreatic beta cells highlights a disease process that is now decipherable at the mechanistic level

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