Change of visfatin, C-reactive protein concentrations, and insulin sensitivity in patients with hyperthyroidism
Introduction
Hyperthyroidism has been linked to reduced lean and fat body mass, resulting in lower-than-normal body weight. Patients with hyperthyroidism often have disrupted intermediary metabolism and thyrotoxicosis that has been associated with insulin resistance [1], [2], [3]. Abnormal levels of adipocytokines (eg, leptin, adiponectin, and resistin) in patients with thyroid dysfunction have been reported [4], [5], [6], [7]. Visfatin, an adipose tissue–derived protein, is known to have insulin-like metabolic effects [8]. The molecule was previously identified as a growth factor for early B-lymphocytes and named as pre-B cell colony-enhancing factor [9]. The gene for visfatin is expressed and regulated in adipocytes [10], [11]. Visfatin gene expression in visceral fat is increased in obese subjects, and the plasma concentration of visfatin has been associated more strongly with the amount of visceral fat than subcutaneous fat [8].
The plasma levels of visfatin in patients with hyperthyroidism due to Graves disease have not been studied. The insulin-like effects of visfatin, such as stimulating glucose transport into muscle cells and adipocytes and inhibiting glucose production in hepatocytes, are dependent on the plasma concentration [8]. Intravenous injection of recombinant visfatin in mice decreases plasma glucose in a dose-dependent fashion [8]. Visfatin appears to play a role in glucose homeostasis and may contribute to the pathogenesis of insulin resistance in hyperthyroidism. In addition, proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor–α (TNF-α) are elevated in Graves disease [12], [13], [14], which may affect insulin sensitivity and interact with visfatin.
The objective of this study was to compare plasma visfatin concentrations in subjects with hyperthyroidism due to Graves disease before and after antithyroid treatment and in euthyoid control subjects. The relationships among visfatin, serum inflammatory marker C-reactive protein (CRP), insulin concentrations, and homeostasis model assessment of insulin resistance index (HOMA-IR) were evaluated.
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Subjects
The study enrolled 19 patients with hyperthyroidism due to Graves disease (14 women and 5 men) and 19 age- and sex-matched euthyroid controls (17 women and 2 men). The diagnosis of Graves disease was made by the presence of circulating thyrotropin receptor antibody (TRAB) in patients with hyperthyroidism. Informed consents were obtained from all subjects after thorough explanation of the procedures. All subjects were free of diabetes mellitus and hypertension. Of the 19 hyperthyroid patients, 8
Results
The demographic and clinical characteristics of the study population are shown in Table 1. The mean ± SEM age was 32.6 ± 1.8 years for hyperthyroid subjects and 36.7 ± 2.7 years for matching control subjects. As expected, subjects in the hyperthyroid group before treatment had lower TSH and higher T3 and FT4 serum concentrations than they did after treatment or the control group. The hyperthyroid group before treatment also had higher visfatin plasma concentrations (20.7 ± 1.8 ng/mL) than they
Discussion
Adipocytokines play a crucial role in the regulation of energy homeostasis, insulin sensitivity, lipid and carbohydrate metabolism, and inflammatory and atherogenic reactions [16], [17], [18], [19], [20], [21], [22]. The adipocytokine visfatin has metabolic effects quantitatively similar to those of insulin [8]. However, the relationship between visfatin and insulin resistance remains inconclusive. One study assessed the association between serum visfatin concentrations and levels of
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