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Leptin, adiponectin, visfatin and retinol-binding protein-4 - mediators of comorbidities in patients with psoriasis?

Abstract：

:White adipose tissue is known to be involved in numerous physiological processes such as insulin-mediated functions, lipid and glucose metabolism, vascular changes and coagulation. These processes are mainly mediated by adipokines that are secreted either from adipocytes or cells of the stromal-vascular fraction of adipose tissue. In obesity, a shift in the production of adipokines can mediate the development of associated diseases, such as metabolic syndrome, and vascular complications, such as artherosclerosis, myocardial infarction or stroke, which are known comorbidities of psoriasis too. As obesity is a frequently seen comorbidity in psoriasis patients, adipokines could be involved in the pathogenesis of psoriasis and/or its comorbidities either dependently or independently from obesity. Therefore, this study investigates the levels of four major adipokines in psoriasis patients compared with a control group of healthy volunteers without chronic inflammatory diseases in relation to body composition. Leptin, adiponectin (high molecular weight (HMW) and total adiponectin), visfatin and retinol-binding protein 4 (RBP4) have been analysed in 79 psoriasis patients and in 80 healthy volunteers. It was shown that HMW adiponectin (OR 1.3755; P = 0.0094) and visfatin (OR 1.1267; P = 0.0472) are independently increased, and RBP4 (OR 0.9884; P < 0.0001) is independently decreased in psoriasis. In conclusion, increased levels of HMW adiponectin and decreased levels of RBP4 could be a mechanism in a chronic inflammatory state that helps to protect against vascular and metabolic disorders, whereas the increase of the pro-inflammatory adipokine visfatin could lead to atherosclerosis and vascular disorders found in psoriasis.

journal_name

Exp Dermatol

journal_title

Experimental dermatology

authors

Gerdes S,Osadtschy S,Rostami-Yazdi M,Buhles N,Weichenthal M,Mrowietz U

doi

10.1111/j.1600-0625.2011.01402.x

subject

Has Abstract

pub_date

2012-01-01 00:00:00

pages

43-7

issue

1

eissn

0906-6705

issn

1600-0625

journal_volume

21

pub_type

杂志文章

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