Lenka Bošanská

Adipokine profile is modulated in subcutaneous adipose tissue by TNFα inhibitors in patients with rheumatoid arthritis

A protective effect of obesity showing that increased adiposity protects against radiographic joint damage in patients with rheumatoid arthritis (RA) has been reported.1 2 Recently, adipokines were suggested as a molecular link explaining this paradoxical association.3,–,5 The levels of serum adiponectin and visfatin have been shown to be associated with increased, radiographic joint damage in RA, while leptin is associated with reduced radiographic joint damage.4 5 Therefore, we tested whether tumour necrosis factor α (TNFα) inhibitor therapy, which prevents joint damage in majority of patients with RA, may be associated with a change in the local production of adipokines in subcutaneous adipose tissue (SAT). SAT samples were obtained from the same abdominal region by aspiration with a bioptic needle in nine patients with RA prior to and 6 months after the treatment with etanercept. Adipose tissue samples were …

Modulation of subcutaneous adipose tissue adipokines by TNF-α blockade therapy in patients with inflammatory arthritides

Objective Increased adiposity has been recently shown to protect against radiographic progression in rheumatoid arthritis (RA). Moreover, low adiponectin serum levels were suggested as mechanistic link between high adiposity and decreased radiographic damage in RA. Therefore, the aim of this study was to examine the hypothesis that beneficial effect of tumour necrosis factor (TNF)-α blockade therapy may be associated with local changes of adipokines in subcutaneous adipose tissue. Methods Samples of subcutaneous adipose tissue for protein analysis were obtained from the same abdominal region in patients with RA (n=9) and ankylosing spondylitis (n=4) prior to and 6 months after the commencement of etanercept. Commercial ELISA assays were used for detection of subcutaneous adipose tissue concentrations of TNF-α, interleukin (IL)-1, IL-6 and adipokines leptin, adiponectin, resistin, visfatin, vaspin and omentin. Western blotting was used to confirm modulated levels of the protein(s). Results Subcutaneous adipose tissue concentrations of IL-1, TNF-α, leptin, resistin, visfatin, vaspin and omentin have not changed during the observation period. However, the levels of adiponectin and IL-6 decreased significantly 6 months following initiation of etanercept therapy (from 35.65±16.45 μg/ml to 15.70±10.40 μg/ml (p=0.003) and from 102.36±45.26 pg/ml to 79.66±31.92 (p=0.049), respectively). This observation was confirmed by western blotting. None of the cytokines or adipokines was associated with serum C-reactive protein. Conclusion Beneficial effect of TNF-α blockade therapy on structural joint damage in patients with inflammatory arthritides may be, at least in part, mediated through the decrease of subcutaneous adipose tissue adiponectin and IL-6.

THE EFFECT OF PHEOCHROMOCYTOMA TREATMENT ON SUBCLINICAL INFLAMMATION AND ENDOCRINE FUNCTION OF ADIPOSE TISSUE

The aim of our study was to evaluate the influence of surgical removal of pheochromocytoma on the endocrine function of adipose tissue and subclinical inflammation as measured by circulating C-reactive protein (CRP) levels. Eighteen patients with newly diagnosed pheochromocytoma were included into study. Anthropometric measures, biochemical parameters, serum CRP, leptin, adiponectin and resistin levels were measured at the time of diagnosis and six months after surgical removal of pheochromocytoma. Surgical removal of pheochromocytoma significantly increased body weight, decreased both systolic and diastolic blood pressure, fasting blood glucose and glycated hemoglobin levels. Serum CRP levels were decreased by 50 % six months after surgical removal of pheochromocytoma (0.49+/-0.12 vs. 0.23+/-0.05 mg/l, p<0.05) despite a significant increase in body weight. Serum leptin, adiponectin and resistin levels were not affected by the surgery. We conclude that increased body weight in patients after surgical removal of pheochromocytoma is accompanied by an attenuation of subclinical inflammation probably due to catecholamine normalization. We failed to demonstrate an involvement of the changes in circulating leptin, adiponectin or resistin levels in this process.