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. 2020 Mar 5;15(3):e0229776. doi: 10.1371/journal.pone.0229776

Fig 1. Summarizes the hypothesis mechanism process of fetuin-A on glucolipid metabolism signaling cascade in MetS.

Fig 1

Fig 1 Schematic representation of the effects of fetuin-A on glucolipid metabolism signaling cascade in MetS that explain positive effects of these factors on glucolipid control. MetS, Metabolic syndrome; Akt: protein kinase b; IL -6: interleukin-6; TNF-α: Tumor Necrosis Factor; AMPK: AMP activated protein-kinase; GLUT: glucose transporter; IRS: insulin receptor substrate; mTOR: mammalian target of rapamicin; APN, adiponectin; PI3K: phosphatidylinositol 3-kinase; mTOR, mechanistic target of rapamycin; NF-κB, nuclear factor κB; ERK 1/2, Extracellular signal-regulated kinases 1 and 2; SREBP- 1C, sterol regulatory element binding protein-1c. Fig 1 is drawn by the KA, without any copyright disputes.