Increased adipose tissue secretion of interleukin-6, but not of leptin, plasminogen activator inhibitor-1 or tumour necrosis factor alpha, in Graves' hyperthyroidism.
OBJECTIVE
This study was designed to investigate adipose tissue secretion of interleukin-6 (IL-6), leptin, tumour necrosis factor alpha (TNF-alpha) and plasminogen activator inhibitor-1 (PAI-1) in Graves' hyperthyroidism.


METHODS
We studied 10 patients before and during (after 8 weeks) anti-thyroid treatment for Graves' hyperthyroidism and 16 healthy, euthyroid control subjects.


METHODS
Plasma levels of thyroid hormones and serum/plasma levels of IL-6, leptin, TNF-alpha and PAI-1 were analysed. Subcutaneous fat biopsies were taken for subsequent measurement of IL-6, leptin, TNF-alpha and PAI-1 protein secretion.


RESULTS
In patients with Graves' disease, the anti-thyroid treatment resulted in significant reductions of plasma thyroxine and triiodothyronine levels. No differences in serum concentration or adipose tissue secretion of leptin or TNF-alpha were observed either before, as compared with during, anti-thyroid treatment, or in comparison with euthyroid controls. In contrast, plasma PAI-1 activity, but not adipose tissue secretion of PAI-1, was increased both in Graves' disease before as compared with during anti-thyroid treatment (P=0.01) and in thyrotoxic patients compared with euthyroid controls (P=0.0001). Finally, adipose secretion of IL-6 was increased both before (8-fold, P=0.001) and during (6-fold, P<0.0001) treatment as compared with control subjects. Accordingly, serum concentration of IL-6 was also increased by about 50% in thyrotoxic patients as compared with healthy controls (P=0.03).


CONCLUSIONS
In Graves' hyperthyroidism regardless of thyroid status, adipose tissue secretion of IL-6, but not of leptin, TNF-alpha or PAI-1, is markedly increased in comparison with euthyroid controls. This suggests that autoimmune thyroidal disorder may regulate adipose tissue release of IL-6.
Wahrenberg
Hans
H
Department of Medicine, Karolinska Institutet, Huddinge University Hospital, Sweden.
Wennlund
Anders
A
Hoffstedt
Johan
J
D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D013956:Antithyroid Agents / Q000627:therapeutic use; D005260:Female; D006111:Graves Disease / Q000188:drug therapy / Q000378:metabolism*; D006801:Humans; D015850:Interleukin-6 / Q000097:blood / Q000378:metabolism*; D020738:Leptin / Q000097:blood / Q000378:metabolism*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood / Q000378:metabolism*; D012016:Reference Values; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D013956:Antithyroid Agents; D015850:Interleukin-6; D020738:Leptin; D017395:Plasminogen Activator Inhibitor 1; D014409:Tumor Necrosis Factor-alpha; D014284:Triiodothyronine; D013974:Thyroxine