Thyroid Hormone Activates Brown Adipose Tissue and Increases Non-Shivering Thermogenesis - A Cohort Study in a Group of Thyroid Carcinoma Patients

Evie Broeders, Guy Vijgen, Bastiaan Havekes, Nicole D. Bouvy, F.M. Mottaghy, M. Kars, N.C. Schaper, Patrick Schrauwen, Boudewijn Brans, Wouter van Marken Lichtenbelt*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

BACKGROUND/OBJECTIVES: Thyroid hormone receptors are present on brown adipose tissue (BAT), indicating a role for thyroid hormone in the regulation of BAT activation. The objective of this study was to examine the effect of thyroid hormone withdrawal followed by thyroid hormone in TSH-suppressive dosages, on energy expenditure and brown adipose tissue activity. SUBJECTS/METHODS: This study was a longitudinal study in an academic center, with a follow-up period of 6 months. Ten patients with well-differentiated thyroid carcinoma eligible for surgical treatment and subsequent radioactive iodine ablation therapy were studied in a hypothyroid state after thyroidectomy and in a subclinical hyperthyroid state (TSH-suppression according to treatment protocol). Paired two-tailed t-tests and linear regression analyses were used. RESULTS: Basal metabolic rate (BMR) was significantly higher after treatment with synthetic thyroid hormone (levothyroxine) than in the hypothyroid state (BMR 3.8 +/- 0.5 kJ/min versus 4.4 +/- 0.6 kJ/min, P = 0.012), and non-shivering thermogenesis (NST) significantly increased from 15 +/- 10% to 25 +/- 6% (P = 0.009). Mean BAT activity was significantly higher in the subclinical hyperthyroid state than in the hypothyroid state (BAT standard uptake value (SUVMean) 4.0 +/- 2.9 versus 2.4 +/- 1.8, P = 0.039). CONCLUSIONS: Our study shows that higher levels of thyroid hormone are associated with a higher level of cold-activated BAT. TRIAL REGISTRATION: ClinicalTrials.gov NCT02499471.
Original languageEnglish
Article numbere0145049
Number of pages15
JournalPLOS ONE
Volume11
Issue number1
DOIs
Publication statusPublished - 19 Jan 2016

Keywords

  • TYPE-2 IODOTHYRONINE DEIODINASE
  • BLOOD-PRESSURE
  • PRIMARY HYPOTHYROIDISM
  • COLD-EXPOSURE
  • HYPERTHYROIDISM
  • HUMANS
  • FAT
  • POPULATION
  • METABOLISM
  • RECEPTOR

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