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It is the intention of this viewpoint to discuss the possible impact of<jats:styled-content style=\"fixed-case\">WD<\/jats:styled-content>\u2010mediated nutrient signalling in the pathogenesis of acne. High glycaemic load and dairy protein consumption both increase insulin\/insulin\u2010like growth factor\u20101 (<jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\u20101) signalling (<jats:styled-content style=\"fixed-case\">IIS<\/jats:styled-content>) that is superimposed on elevated<jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\u20101 signalling of puberty. The cell's nutritional status is primarily sensed by the forkhead box transcription factor<jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>1 (<jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>ox<jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>1) and the serine\/threonine kinase mammalian target of rapamycin complex 1 (m<jats:styled-content style=\"fixed-case\">TORC<\/jats:styled-content>1). Increased<jats:styled-content style=\"fixed-case\">IIS<\/jats:styled-content>extrudes<jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>ox<jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>1 into the cytoplasm, whereas nuclear<jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>ox<jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>1 suppresses hepatic<jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\u20101 synthesis and thus impairs somatic growth.<jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>ox<jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>1 attenuates androgen signalling, interacts with regulatory proteins important for sebaceous lipogenesis, regulates the activity of innate and adaptive immunity, antagonizes oxidative stress and most importantly functions as a rheostat of m<jats:styled-content style=\"fixed-case\">TORC<\/jats:styled-content>1, the master regulator of cell growth, proliferation and metabolic homoeostasis. Thus,<jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>ox<jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>1 links nutrient availability to m<jats:styled-content style=\"fixed-case\">TORC<\/jats:styled-content>1\u2010driven processes: increased protein and lipid synthesis, cell proliferation, cell differentiation including hyperproliferation of acroinfundibular keratinocytes, sebaceous gland hyperplasia, increased sebaceous lipogenesis, insulin resistance and increased body mass index. Enhanced androgen,<jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1 and<jats:styled-content style=\"fixed-case\">IGF<\/jats:styled-content>\u20101 signalling due to genetic polymorphisms promoting the risk of acne all converge in m<jats:styled-content style=\"fixed-case\">TORC<\/jats:styled-content>1 activation, which is further enhanced by nutrient signalling of<jats:styled-content style=\"fixed-case\">WD<\/jats:styled-content>. Deeper insights into the molecular interplay of<jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>ox<jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>1\/m<jats:styled-content style=\"fixed-case\">TORC<\/jats:styled-content>1\u2010mediated nutrient signalling are thus of critical importance to understand the impact of<jats:styled-content style=\"fixed-case\">WD<\/jats:styled-content>on the promotion of epidemic acne and more serious m<jats:styled-content style=\"fixed-case\">TORC<\/jats:styled-content>1\u2010driven diseases of civilization.<\/jats:p>","DOI":"10.1111\/exd.12142","type":"journal-article","created":{"date-parts":[[2013,3,23]],"date-time":"2013-03-23T22:02:41Z","timestamp":1364076161000},"page":"311-315","source":"Crossref","is-referenced-by-count":144,"title":["Potential role of<scp>F<\/scp>ox<scp>O<\/scp>1 and m<scp>TORC<\/scp>1 in the pathogenesis of<scp>W<\/scp>estern diet\u2010induced 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