We performed prospective study in women with severe thyroid dysfunctions of autoimmune origin, and we found that restoration of euthyroidism is associated with alterations in body composition. Hyperthyroid women gained weight, mainly due to increase of fat mass in trunk and limbs, while muscle mass remained unaltered. Significant increase of fat mass in hyperthyroid females was followed by the increase of visfatin concentration after the treatment. There is limited number of studies evaluating the changes in body composition during anti-thyroid therapy, especially taking into account an estimation of regional body mass distribution with a subdivision to limbs and trunk. Significant increase in fat mass during restoration of thyroid function was reported also by other authors (2). However, in contrast to our findings some studies described increase in muscle mass when euthyroidism was achieved (2, 16). What more, clinical improvement of muscle strength has been noted after restoration of thyroid function in subclinical and overt hyperthyroidism (16). Observed muscle weakness in hyperthyroid patients mainly results from changes in skeletal muscle metabolism with no muscle cells destruction, therefore post-therapeutic muscle mass might remain similar (17). We have performed a study solely among women, and similar influence of normalization of thyroid function on body composition parameters, including fat and muscle masses in Graves’ hyperthyroidism has been recently reported by other authors (18). Weight loss in hypothyroid females in current study is a result of the decrease in both fat and muscle masses. Similar reduction of adiposity have been observed by other authors (2, 19). Interestingly, one study reported that the decrease of body weight was caused mainly by the decrease of lean mass, while fat mass remained unaltered during the therapy (20). One may suggest, that differences in physical activity during the therapy might explain observed differences. Observed metabolic and anthropometric changes after the restoration of thyroid function in both hyper- and hypothyroid patients might not be accompanied by normalization of energy expenditure. Levothyroxine-replacement therapy causing decrease of FT3 levels has been proved to be associated with lowering of FT3-dependent resting energy expenditure in contrast to healthy controls (21). Recent systemic review and meta-analysis found that normalization of TSH in levothyroxine-treated patients does not lead to sufficient decrease of low dose lipoprotein and total cholesterol levels (22). These effects might be clinically significant not only for patients primarily treated with levothyroxine because of hypothyroidism, but also for initially hyperthyroid subjects who needed radical therapy with radioiodine or thyroidectomy followed by necessity of levothyroxine substitution. Therefore, prevention of unfavourable anthropometric changes observed during the therapy of thyroid dysfunctions could have beneficial metabolic effects.
Total body adiposity was the major determinant of visfatin concentrations in females with thyroid dysfunctions of autoimmune origin, but jet fat trunk or visceral fat index did not correlate with its concentration. This observation is in line with other studies suggesting that subcutaneous fat tissue contributes well to circulating visfatin level (23, 24). Our findings might also explain contradictory results of other studies applying traditional methods for anthropometric assessment (i.e. body mass index, waist-to-hip ratio, or skin fold) (25, 26). We have confirmed our previous findings that serum visfatin correlates with TPOAbs in hypothyroid patients, which has been recently also reported in children (27). Likewise, Caixas at al. observed that in hyperthyroid patients fat mass increases during the therapy with concomitant increase of visfatin (9). The design of our study limits our possibilities to conclude whether observed visfatin changes during recovery in hyperthyroid females simply reflect increase of adiposity or is a compensatory response involved in glucose regulation. On the other hand, since TSH receptor is expressed in adipocytes, observed changes might result from TSH receptor stimulation in fat tissue potentially leading to release of visfatin (28). In contrast to other authors, visfatin remained unchanged after recovery in hypothyroid women (9). Visfatin has been suggested to act as a myokine, and in some studies levothyroxine substitution lead to increment of muscle mass (29). We have noticed significant decrease of muscle mass during the therapy, and this difference might explain contradictory results.
The main objective and novelty of our study is the prospective analysis of the link between visfatin, thyroid-related hormones and antithyroid antibodies levels, as well as body composition parameters, including fat content and muscle mass in trunk and limbs. What is more, to the best of our knowledge, this is the first study investigating serum visfatin changes in three different thyrometabolic states in the same individuals. The main limitation of our study is the use of bioimpedance method for body composition analysis, which is not as precise as Dual-energy X-ray absorptiometry (DXA). However, accuracy of bioimpedance has been already proved in several studies, also among patients with thyroid dysfunctions (30). What is more, we applied strict inclusion and exclusion criteria, which allowed us to provide more accurate results. Finally, we followed the same patients during the therapy, which limited the influence of individual factors.