Abstract
Resistin, belongs to cysteine-rich secretory protein, is mainly produced by circulating leukocytes, such as neutrophils monocytes and macrophages in humans. To date, few but controversial studies have reported about resistin concentrations in hyperthyroid patients, especially in Graves' disease (GD). We undertaked a controlled, prospective study to explore the serum resistin concentration in GD patients before and after -MMI treatment. In addition, we also investigated the main influencing factor on serum resistin level and discuessed the potential role of serum resistin plays in GD patients. 39 untreated GD (uGD) patients, including 8 males and 31 females, were enrolled in our investigation. All of these patients were prescribed with MMI treatment, in addition to 25 healthy controls. Anthropometric parameters and hormone assessment were measured. Enzyme-linked immunosorbent assay was used to detect serum resistin concentration in different stages of GD patients. Furthermore, neutrophil cell line NB4 with or without T3 treatment to detect the effect of thyroid hormones on resistin expression. The serum resistin level and neutrophil counts in untreated GD patients were significantly declined. And all of these parameters were recovered to normal after MMI treatment in ethyroid GD (eGD) and TRAb-negative conversion (nGD) patients. Resistin concentration exhibited a negative correlation with FT3 and FT4, but a positive correlation with absolute number of neutrophiles in uGD patients, whereas did not correlate with thyroid autoimmune antibodies and BMI. Neutrophile cell line, NB4, produced decreased expression of resistin when stimulated with T3. Our study showed a decrease of serum resistin level in GD patients and we suggested that the serum resistin might primarily secreted from circulating neutrophils and down-regulated by excessive thyroid hormones in GD patients.
Highlights
Resistin, named by Steppan et al in virtue of its crucial role in insulin resistance in mice, is a serine/cysterin-rich secretory protein [1, 2]
Our study showed a decrease of serum resistin level in Graves’ disease (GD) patients and we suggested that the serum resistin might primarily secreted from circulating neutrophils and down-regulated by excessive thyroid hormones in GD patients
The results showed that both neutrophile proportion (Neu%) (51.18±7.19 vs 58.34±6.84; p=0.02) and neutrophile count (NEUT) (2.95±0.97×106 vs 3.75±1.04×106; p=0.007) were declined in untreated GD (uGD) patients and recovered in ethyroid GD (eGD) (Neu%: 55.63±7.72; NEUT: 3.50±1.05×106) and negative GD (nGD) (Neu%: 59.04±5.83; NEUT: 3.74±1.48×106) (Figure 2A)
Summary
Resistin, named by Steppan et al in virtue of its crucial role in insulin resistance (resist to insulin) in mice, is a serine/cysterin-rich secretory protein [1, 2]. In rodents, it is primarily produced in adipocytes and influenced by genetic and diet, causing increased release of resistin in mouse models of obesity [3]. First and foremost, human resistin is primarily secreted from inflammatory cells, such as monocytes and neutrophils, whereas micro-concentration in human adipocytes [9, 10]. Though associated with obesity and diabetes in population studies, resistin is thought to be www.impactjournals.com/oncotarget
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