Investigation of the Relationship between MR-Based Supraclavicular Fat Fraction and Thyroid Hormones

Abstract

Purpose: Brown adipose tissue (BAT) plays a potential role in energy and glucose metabolism in humans. Thyroid hormones (TH) are main regulators of BAT development and function. However, it remains unknown how the magnetic resonance (MR)-based proton density fat fraction (PDFF) of supraclavicular adipose tissue used as a surrogate marker for BAT presence relates to TH. Therefore, the purpose of this analysis was to investigate the relationship between supraclavicular PDFF and serum levels of TH. Methods: In total, 96 adult volunteers from a large cross-sectional study who underwent additional MR examination of the neck and pelvis were included in this analysis. Segmented PDFF maps of the supraclavicular and gluteal subcutaneous adipose tissue were generated. Delta PDFF was calculated as the difference between gluteal and supraclavicular PDFF and grouped as high (≥12%) or low (<12%) based on the median and the clinical rationale of a high versus low probability of BAT being present. Thyroid-stimulating hormone (mIU/L), free triiodothyronine (FT3, pg/mL) and free thyroxine (FT4, ng/dL) levels were determined in blood samples. Body mass index (BMI) was calculated as weight (kg)/height (m)². Statistical analyses included the use of paired samples ttest, simple linear regression analysis and a multivariable linear regression analysis. Results: The median age of the subjects (77% female) was 33 years, BMI ranged from 17.2 to 43.1 kg/m². Supraclavicular and gluteal PDFF differed significantly (76.5 ± 4.8 vs. 89.4 ± 3.5 %, p < 0.01). Supraclavicular PDFF was associated with FT3 in subjects with high delta PDFF (R² = 0.17, p < 0.01), with higher FT3 being associated with lower supraclavicular PDFF (y = 85.2 + –3.6 x). In a multivariable linear regression analysis considering further potential prognostic factors, the interaction between the delta PDFF group and FT3 remained a predictor for supraclavicular PDFF (B = –4.65, p < 0.01). Discussion/Conclusions: Supraclavicular PDFF corresponds to the presence of BAT. In the present analysis, supraclavicular PDFF is correlated with FT3 in subjects with high delta PDFF. Therefore, the present findings suggest that biologically active T3 may be involved in the development of supraclavicular BAT.

Metabolic effects of brown fat in transitioning from hyperthyroidism to euthyroidism

“…In our previous study, we had reported that FT3 level at baseline was significantly higher in BAT-positive healthy participants than BAT-negative participants 56 . Junker et al 57 reported biologically active T3 may be involved in the development of supraclavicular BAT.…”

“…In our previous study, we had reported that FT3 level at baseline was significantly higher in BAT-positive healthy participants than BAT-negative participants ( 55 ). Junker et al ( 56 ) reported that biologically active T3 may be involved in the development of supraclavicular BAT. In our current study, we also found that circulating FT3 concentration was significantly higher in BAT-positive patients compared to BAT-negative patients in both the hyperthyroid and euthyroid states.…”

Brown Adipose Tissue—A Translational Perspective

“…However, these acute changes in circulating T4 and TSH levels are of unclear clinical significance. Higher serum T3 levels were found in cold-induced 18 FDG BAT–positive individuals in one study ( 406 ) and with lower BAT fat fraction on MRI in another ( 408 ). A positive association between serum free T4 levels and cold-induced BAT glucose uptake was found in 24 euthyroid and healthy participants ( 409 ).…”

Deficiency of lipopolysaccharide binding protein facilitates adipose browning, glucose uptake and oxygen consumption in mouse embryonic fibroblasts via activating PI3K/Akt/mTOR pathway and inhibiting autophagy

“…To explore the roles of LBP in adipose browning and metabolism, MEFs were induced to differentiate into adipocytes with BAT-like characteristics, and the transfection of shLBP was made to establish the model of gene silence at the same time. Located in mitochondria, UCP-1 is a characteristic protein of BAT, which fulfills a crucial function on the release of energy in the form of heat (thermogenesis) through uncoupling oxidative phosphorylation from synthesized adenosine triphosphate (ATP) [ 49 ]. A prominent upregulation of the UCP-1 level has been exhibited in LBP-null mice and adipocytes treated with the silence of LBP [ 40 ].…”