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. 2013 Apr 25;22(5):311–315. doi: 10.1111/exd.12142

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© 2013 John Wiley & Sons A/S

Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.

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Increased insulin/IGF-1 signalling (IIS) of Western diet (WD) results in Akt-mediated FoxO1 inhibition by nuclear extrusion. Akt-mediated phosphorylation of TSC2 attenuates the inhibitory effect of TSC1/TSC2 on Rheb, thus promotes mTORC1 activation. In contrast, nuclear activation of FoxO1 stimulates the expression of sestrin3, which via AMPK activation inhibits mTORC1. Increased IIS of WD is superimposed on enhanced IIS of puberty, thereby promotes the development of acne. FoxO1 inhibits GHR expression, hepatic IGF-1 synthesis and androgen receptor (AR) transactivation. GIP, glucose-dependent insulinotropic polypeptide; GH, growth hormone; GHR, GH receptor; Leu, leucine; LAT, L-type amino acid transporter; IR, insulin receptor; IRS, insulin receptor substrate; PI3K, phosphoinositol-3 kinase; Akt, Akt kinase (protein kinase B); FoxO, forkhead box transcription factor class O; TSC, tuberous sclerosis complex; Rheb, ras-homolog enriched in brain; mTORC1, mammalian target of rapamycin complex 1; AMPK, AMP kinase; T, testosterone; DHT, dihydrotestosterone.