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. 2015 Oct 20;9:5727–5736. doi: 10.2147/DDDT.S92355

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© 2015 Gao et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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The targets of 4-HIL action identified in the current study.

Notes: The role of 4-HIL in the crosstalk between the inflammatory cytokine TNF-α and the insulin signaling pathway can be described using the following five key steps: (a) the down regulation of TNF-α-converting enzyme (TACE) expression; (b) inhibiting the phosphorylation of IRS-1 at Ser³⁰⁷; (c) inhibiting the phosphorylation of Akt at Ser⁴⁷³; (d) the upregulation of glucose transporter-4 (GLUT4) expression at the cellular membrane.

Abbreviations: 4-HIL, (2S,3R,4S)-4-hydroxyisoleucine; TNF-α, tumor necrosis factor-α; IRS-1, insulin receptor substrate-1, PPAR, peroxisome proliferator-activated receptor; PIO, pioglitazone; sTNF-α, soluble TNF-α; TNFR-I, tumor necrosis factor-α receptor I.