TSH suppression aggravates arterial inflammation - an F-FDG PET study in thyroid carcinoma patients.

Purpose: We aimed to investigate the influence of both hypothyroidism and thyroid-stimulating hormone (TSH) suppression on vascular inflammation, as assessed with F-fluorodeoxyglucose (F-FDG) positron emission tomography (PET)/computed tomography (CT).

Methods: Ten thyroid carcinoma patients underwent an F-FDG PET/CT during post-thyroidectomy hypothyroidism and during thyrotropin (TSH) suppression after I (radioiodine) ablation therapy. We analysed the F-FDG uptake in the carotids, aortic arch, ascending, descending, and abdominal aorta to investigate the effects of thyroid hormone status on arterial inflammation.

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

[This corrects the article DOI: 10.1371/journal.pone.

Genetic Markers of Brown Adipose Tissue Identity and In Vitro Brown Adipose Tissue Activity in Humans.

Objective: Human brown adipose tissue (BAT) activity decreases with age and obesity. In addition to uncoupling protein 1 (UCP1), several genetic markers of BAT in humans have been published. However, the link between human BAT activity and genetic markers has been inadequately explored.

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

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.

The Bile Acid Chenodeoxycholic Acid Increases Human Brown Adipose Tissue Activity.

The interest in brown adipose tissue (BAT) as a target to combat metabolic disease has recently been renewed with the discovery of functional BAT in humans. In rodents, BAT can be activated by bile acids, which activate type 2 iodothyronine deiodinase (D2) in BAT via the G-coupled protein receptor TGR5, resulting in increased oxygen consumption and energy expenditure. Here we examined the effects of oral supplementation of the bile acid chenodeoxycholic acid (CDCA) on human BAT activity.