Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2015) 37 GP25.02 | DOI: 10.1530/endoabs.37.GP.25.02

ECE2015 Guided Posters Thyroid – nodule (7 abstracts)

Thyroid hormones influence the expression of TNF-related apoptosis-inducing ligand

Stella Bernardi 1, , Fleur Bossi 1 , Fabiola Giudici 1 , Paola Secchiero 2 , Giorgio Zauli 3 & Bruno Fabris 1


1Department of Medical, Surgical, Health Sciences, University of Trieste, Trieste, Italy; 2Department of Morphology, Surgery, and Experimental Medicine, LTTA Center, University of Ferrara, Ferrara, Italy; 3Institute for Maternal and Child Health, IRCCS ‘Burlo Garofolo’, Trieste, Italy.


Background: There is growing evidence supporting TNF-related apoptosis-inducing ligand (TRAIL) involvement in weight and body composition regulation, which are classically influenced by thyroid hormones. This study aimed at investigating the relationship between thyroid hormones and TRAIL.

Methods: Circulating TRAIL was measured in 40 controls, 40 hyperthyroid, and 25 hypothyroid patients before and after their respective treatments. In the same patients TRAIL gene expression was quantified in peripheral blood mononuclear cells. The effect of T3 and T4 on TRAIL secretion was evaluated in vitro.

Results: TRAIL gene and protein expression significantly increased in hyperthyroid and decreased in hypothyroid patients (vs controls P<0.05). TRAIL gene and protein expression normalized once euthyroidism was restored (P<0.05). There was a significant correlation between TRAIL and both T3 and T4 (P<0.05). Moreover, the changes in body weight and BMI that we found once euthyroidism was restored were significantly correlated to the changes in TRAIL (P<0.05). The in vitro study showed that T3 stimulated TRAIL release in a dose-dependent manner.

Conclusion: These findings are consistent with the view that TRAIL might be involved in body weight regulation. In addition, this work sheds light on the possibility that TRAIL might be one of the molecules mediating thyroid hormone peripheral effects.

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