title: Visfatin plasma concentrations in patients with hyperthyroidism and hypothyroidism before and after control of thyroid function.
abstract: Alterations in thyroid function are associated with changes in body weight, metabolism, and low-grade inflammation. In several studies, plasma levels of visfatin were found to be associated with body mass index, diabetes, and metabolic syndrome. In our study we aimed to evaluate visfatin levels according to thyroid dysfunction. The study cohort comprised 56 Hashimoto thyroiditis patients with hypothyroidism (43.94+/-14.27 yr), 56 Graves patients with hyperthyroidism (45.87+/-13.28 yr), and 56 euthyroid healthy subjects (45.23+/-7.11 yr) as a control group. In addition, we evaluated the effect of therapy on plasma visfatin levels in 16 hypothyroid and in 25 hyperthyroid patients. Markedly low visfatin levels were found in hyperthyroid patients [9.44 (8.07- 10.8) ng/ml] compared with the hypothyroid [49.93 (40.72- 59.1) ng/ml] and control groups [38.6 (30.6-46.6) ng/ml] (p<0.001, p<0.001). Plasma visfatin levels in patients with hypothyroidism decreased significantly following treatment [58.58 (10.21-190.7) ng/ml vs 40.00 (10.01-102.6) ng/ml; p=0.001]. Plasma visfatin levels increased significantly after antithyroid therapy in patients with hyperthyroidism [7.86 (1.02-19.23) ng/ml vs 12.63 (3.48-110.9) ng/ml; p<0.001]. There were negative correlations between visfatin levels with free T3 (r=-0.719, p<0.001), and free T4 (r=-0.716, p<0.001) levels. There was a positive correlation between visfatin and TSH levels (r=0.701, p<0.001). There was a negative correlation between delta visfatin levels with delta free T3, delta free T4 (r=-0.686, p<0.001; r=-0.624, p<0.001). Visfatin thus seems to be regulated by thyroid hormones. While the influence of thyroid dysfunction on adipocytokine production and release is still poorly understood, the results of our study suggest that the effects of hyper- and hypothyroidism on various metabolic parameters may be partly mediated by visfatin.
authors.affiliation: Department of Endocrinology and Metabolism, Maras Sutcuimam School of Medicine, Kahramanmaras, Turkey.
authors.forename: M
authors.initials: M
authors.lastname: Ozkaya
authors.forename: M
authors.initials: M
authors.lastname: Sahin
authors.forename: E
authors.initials: E
authors.lastname: Cakal
authors.forename: F
authors.initials: F
authors.lastname: Yuzbasioglu
authors.forename: K
authors.initials: K
authors.lastname: Sezer
authors.forename: M
authors.initials: M
authors.lastname: Kilinc
authors.forename: S Simsek
authors.initials: SS
authors.lastname: Imrek
mesh_terms: D000328:Adult; D013956:Antithyroid Agents / Q000008:administration & dosage; D003430:Cross-Sectional Studies; D016207:Cytokines / Q000097:blood* / Q000502:physiology; D005260:Female; D020249:Hormone Replacement Therapy; D006801:Humans; D006980:Hyperthyroidism / Q000097:blood* / Q000188:drug therapy* / Q000503:physiopathology; D007037:Hypothyroidism / Q000097:blood* / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood* / Q000502:physiology; D009994:Osmolar Concentration; D011433:Propranolol / Q000008:administration & dosage*; D011441:Propylthiouracil / Q000008:administration & dosage*; D020127:Recovery of Function / Q000502:physiology; D013961:Thyroid Gland / Q000187:drug effects / Q000503:physiopathology; D013974:Thyroxine / Q000627:therapeutic use*
chemical_list: D013956:Antithyroid Agents; D016207:Cytokines; D011441:Propylthiouracil; D011433:Propranolol; D054409:Nicotinamide Phosphoribosyltransferase; C085455:nicotinamide phosphoribosyltransferase, human; D013974:Thyroxine