High-fat diet exacerbates inflammation and cell survival signals in the skin of ultraviolet B-irradiated C57BL/6 mice

Toxicol Appl Pharmacol. 2009 Dec 15;241(3):303-10. doi: 10.1016/j.taap.2009.09.003. Epub 2009 Sep 9.


Inflammation induced by chronic exposure to ultraviolet (UV) radiation has been implicated in various skin diseases. We formulated the hypothesis that a high-fat diet may influence the UV-induced inflammatory responses in the skin. C57BL/6 mice were fed a high-fat diet or control diet and exposed to UVB radiation (120 mJ/cm(2)) three times/week for 10 weeks. The mice were then sacrificed and skin and plasma samples collected for analysis of biomarkers of inflammatory responses using immunohistochemistry, western blotting, ELISA and real-time PCR. We found that the levels of inflammatory biomarkers were increased in the UVB-exposed skin of the mice fed the high-fat diet than the UVB-exposed skin of the mice fed the control diet. The levels of inflammatory biomarkers of early responses to UVB exposure (e.g., myeloperoxidase, cyclooxygenase-2, prostaglandin-E(2)), proinflammatory cytokines (i.e., tumor necrosis factor-alpha, interleukin-1beta, interleukin-6), and proliferating cell nuclear antigen and cell survival signals (phosphatidylinositol-3-kinase and p-Akt-Ser(473)) were higher in high-fat-diet-fed mouse skin than control-diet-fed mouse skin. The plasma levels of insulin growth factor-1 were greater in the UVB-irradiated mice fed the high-fat diet than the UVB-irradiated mice fed the control diet, whereas the levels of plasma adiponectin were significantly lower. This pronounced exacerbation of the UVB-induced inflammatory responses in the skin of mice fed a high-fat diet suggests that high-fat diet may increase susceptibility to inflammation-associated skin diseases, including the risk of skin cancer.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Adiponectin / blood
  • Animals
  • Apoptosis / drug effects
  • Biomarkers
  • Blotting, Western
  • Cell Survival / drug effects*
  • Cell Survival / radiation effects*
  • Cyclooxygenase 2 / biosynthesis
  • Diet
  • Dietary Fats / toxicity*
  • Dinoprostone / biosynthesis
  • Female
  • Immunoenzyme Techniques
  • In Situ Nick-End Labeling
  • Inflammation / chemically induced
  • Inflammation / pathology*
  • Insulin-Like Growth Factor I / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Neutrophil Infiltration / drug effects
  • Oncogene Protein v-akt / biosynthesis
  • Peroxidase / metabolism
  • Phosphatidylinositol 3-Kinases / biosynthesis
  • Skin / cytology
  • Skin / drug effects
  • Skin / radiation effects
  • Ultraviolet Rays*
  • Weight Gain / drug effects


  • Adiponectin
  • Biomarkers
  • Dietary Fats
  • Insulin-Like Growth Factor I
  • Peroxidase
  • Cyclooxygenase 2
  • Phosphatidylinositol 3-Kinases
  • Oncogene Protein v-akt
  • Dinoprostone