High fat diet (HFD) has been implicated in a metabolic syndrome that combines several set of diseases such as Type II diabetes, obesity, etc. Frequently, metabolic syndrome is associated with skin inflammation (acne, dermatitis, etc). Mechanism is unknown.
A new paper in journal Immunity provided results that indicate that epidermal fatty acid binding protein, E-FABP, is a direct link between skin inflammation and HFD.
This is a simple, observation-type of research. I would say that the authors were lucky to get it published in Immunity. Though, I liked the idea that the authors developed the concept for the paper through serendipitous observation.
Initially, the authors showed in their mouse facility, B6 mouse strain fed HFD for 3-6 months developed skin lesions that correlated with fat content in the diet.
Next, the authors found that lesion skin from HFD-fed mice contained higher proportion of macrophages.
These macrophages from lesion skin tend to produce high levels of IL-1β and IL-18.
Analysis of E-FABP expression (fatty acid chaperons) showed its up-regulation in lesion skin and macrophages from HFD-fed mice.
Finally, using E-FABP knockout mice, the authors showed that absence of E-FABP prevented development of skin lesions in HFD-fed mice (with no effect on weight gain).
In summary, these results indicate that excess of dietary fat (saturated fat) induces skin inflammation via epidermal fatty acid binding protein. The authors think it has to do with activation of NALP3 pathway in macrophages by excess saturated fat (leading to IL-1β and IL-18 production) and recruitment of T cells secreting IFN-γ and IL-17 (though those are correlative results and not particularly persuasive). However, effect of E-FABP on skin lesion development is striking.
David Usharauli
Analysis of E-FABP expression (fatty acid chaperons) showed its up-regulation in lesion skin and macrophages from HFD-fed mice.
Finally, using E-FABP knockout mice, the authors showed that absence of E-FABP prevented development of skin lesions in HFD-fed mice (with no effect on weight gain).
In summary, these results indicate that excess of dietary fat (saturated fat) induces skin inflammation via epidermal fatty acid binding protein. The authors think it has to do with activation of NALP3 pathway in macrophages by excess saturated fat (leading to IL-1β and IL-18 production) and recruitment of T cells secreting IFN-γ and IL-17 (though those are correlative results and not particularly persuasive). However, effect of E-FABP on skin lesion development is striking.
David Usharauli
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