Abstract
Ulcerative dermatitis (UD) is a severe inflammatory skin disorder with an unknown aetiology. Recently, insulin receptor substrate 1 KO mice were shown to be fully resistant to UD. In this study, we showed that high-fat diet (HFD) feeding significantly increased incidence of UD in wild type (WT) C57BL/6 mice, as did lithium-mediated inhibition of GSK3-β, which is a key negative regulator of IRS1. In contrast to WT mice, resistance to UD was fully preserved in HFD-fed Irs1-KO mice. Our results identify IRS1 as a key determinant of UD pathogenesis and establish a direct link between diet composition, obesity-induced inflammation and chronic ulceration.
© 2012 John Wiley & Sons A/S.
Publication types
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Letter
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Dermatitis / complications
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Dermatitis / etiology*
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Dermatitis / metabolism
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Dietary Fats / administration & dosage*
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Dietary Fats / adverse effects
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Glycogen Synthase Kinase 3 / drug effects
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Glycogen Synthase Kinase 3 / metabolism*
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Glycogen Synthase Kinase 3 beta
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Insulin Receptor Substrate Proteins / genetics
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Insulin Receptor Substrate Proteins / metabolism*
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Lithium / pharmacology
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Risk Factors
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Signal Transduction
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Skin Ulcer / complications
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Skin Ulcer / etiology*
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Skin Ulcer / metabolism
Substances
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Dietary Fats
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Insulin Receptor Substrate Proteins
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Irs1 protein, mouse
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Lithium
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Glycogen Synthase Kinase 3 beta
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Glycogen Synthase Kinase 3