A.R. Shipman; G.W.M. Millington

Disclosures

The British Journal of Dermatology. 2011;165(4):743-750. 

In This Article

Adipocytokines, Obesity and Psoriasis

Macrophages in adipose tissue produce TNF-α, as well as other cytokines involved in psoriasis, such as IL-1, IL-6, IL-17 and interferon-γ.[5,60] These adipocytokines, as well as leptin, are recruited and stimulated in obesity and may have an autocrine and paracrine effect on nearby skin.[5,29,60] Leptin, produced by adipocytes,[13] decreases T-cell autoregulation and is involved in inflammatory processes stimulating cytokine release,[28] as well as its more established role in appetite suppression and metabolic control.[27] Leptin levels have been shown to correlate with psoriasis severity.[61] Resistin is also produced in adipose tissue and leads to insulin resistance and upregulation of inflammatory processes including TNF-α secretion.[62,63] Resistin levels are increased in patients with psoriasis, correlating with obesity and increased severity of psoriasis.[62,63] Similarly, levels of adiponectin (an anti-inflammatory mediator produced by adipocytes that reduces oxidative stress) are lower in the obese psoriatic compared with the nonobese psoriatic and the inverse is true of interleukin.[13,64,65]

Thus, there is some indirect evidence that the immunological and metabolic alterations associated with obesity may be linked with the pathophysiology of psoriasis.[5,13,27–29,60–65] This is supported by the series of clinical observations that obesity does not appear to impair the treatment of psoriasis, except when treatments with the newer biologic therapies (that block cytokines) are being used.[5]

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