Key result
18F-FDG PET/CT successfully monitors β3 agonist-induced brown adipocyte recruitment in mice, correlating with UCP1 content.
Why the study?
There is rising interest in recruitment of brown adipocytes into white adipose tissue to augment energy expenditure for weight reduction, but imaging biomarkers to monitor this process are needed.
Does 18F-FDG PET/CT accurately monitor brown adipocyte recruitment into white adipose tissue in C57BL/6 mice treated with a β3 agonist?
Does 18F-FDG PET/CT accurately monitor brown adipocyte recruitment into white adipose tissue in C57BL/6 mice treated with a β3 agonist?
18F-FDG PET/CT can effectively monitor the recruitment of brown adipocytes into white adipose tissue in vivo, serving as a potential imaging biomarker for weight reduction strategies.
Hypothesis-generating in mice for 18F-FDG PET/CT as a beige fat biomarker; leaves open human translation for obesity therapies.
UNLABELLED: There is rising interest in recruitment of brown adipocytes into white adipose tissue (WAT) as a means to augment energy expenditure for weight reduction. We thus investigated the potential of (18)F-FDG uptake as an imaging biomarker that can monitor the process of WAT browning. METHODS: C57BL/6 mice were treated daily with the β3 agonist CL316,243 (5-[(2R)-2-[[(2R)-2-(3-chlorophenyl)-2-hydroxyethyl]amino]propyl]-1,3-benzodioxole-2,2-dicarboxylic acid disodium salt), whereas controls received saline. (18)F-FDG small-animal PET/CT was serially performed at 1 h after CL316,243 injection. After sacrifice, interscapular brown adipose tissue (BAT) and WAT depots were extracted, weighed, and measured for (18)F-FDG uptake. Tissues underwent immunostaining, and UCP1 content was quantified by Western blotting. RESULTS: PET/CT showed low (18)F-FDG uptake in both BAT and inguinal WAT at baseline. BAT uptake was substantially increased by a single stimulation with CL316,243. Uptake in inguinal WAT was only modestly elevated by the first stimulation uptake but gradually increased to BAT level by prolonged stimulation. Ex vivo measurements recapitulated the PET findings, and measured (18)F-FDG uptake in other WAT depots was similar to inguinal WAT. WAT browning by prolonged stimulation was confirmed by a substantial increase in uncoupling protein 1 (UCP1), cytochrome-c oxidase 4 (COX4), and PR domain containing 16 (PRDM16) staining as markers of brown adipocytes. UCP1 content, which served as a measure for extent of browning, was low in baseline inguinal WAT but linearly increased over 10 d of CL316,243 injection. Finally, image-based and ex vivo-measured (18)F-FDG uptake in inguinal WAT correlated well with UCP1 content. CONCLUSION: (18)F-FDG PET/CT has the capacity to monitor brown adipocyte recruitment into WAT depots in vivo and may thus be useful for screening the efficacy of strategies to promote WAT browning.
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Park et al. (2014) studied this question. β3 agonist CL316,243 vs. saline was evaluated on 18F-FDG uptake and UCP1 content. 18F-FDG PET/CT successfully monitored brown adipocyte recruitment into white adipose tissue in mice treated with the β3 agonist CL316,243, with uptake correlating well with UCP1 content.
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