RT Journal Article
SR Electronic
T1 Dissociation Between Brown Adipose Tissue <sup>18</sup>F-FDG Uptake and Thermogenesis in Uncoupling Protein 1–Deficient Mice
JF Journal of Nuclear Medicine
JO J Nucl Med
FD Society of Nuclear Medicine
SP 1100
OP 1103
DO 10.2967/jnumed.116.186460
VO 58
IS 7
A1 Hankir, Mohammed K.
A1 Kranz, Mathias
A1 Keipert, Susanne
A1 Weiner, Juliane
A1 Andreasen, Sille G.
A1 Kern, Matthias
A1 Patt, Marianne
A1 Klöting, Nora
A1 Heiker, John T.
A1 Brust, Peter
A1 Hesse, Swen
A1 Jastroch, Martin
A1 Fenske, Wiebke K.
YR 2017
UL http://jnm.snmjournals.org/content/58/7/1100.abstract
AB 18F-FDG PET imaging is routinely used to investigate brown adipose tissue (BAT) thermogenesis, which requires mitochondrial uncoupling protein 1 (UCP1). It remains uncertain, however, whether BAT 18F-FDG uptake is a reliable surrogate measure of UCP1-mediated heat production. Methods: UCP1 knockout (KO) and wild-type (WT) mice housed at thermoneutrality were treated with the selective β3 adrenergic receptor agonist CL 316, 243 and underwent metabolic cage, infrared thermal imaging and 18F-FDG PET/MRI experiments. Primary brown adipocytes were additionally examined for their bioenergetics by extracellular flux analysis as well as their uptake of 2-deoxy-3H-glucose. Results: In response to CL 316, 243 treatments, oxygen consumption, and BAT thermogenesis were diminished in UCP1 KO mice, but BAT 18F-FDG uptake was fully retained. Isolated UCP1 KO brown adipocytes exhibited defective induction of uncoupled respiration whereas their glycolytic flux and 2-deoxy-3H-glucose uptake rates were largely unaffected. Conclusion: Adrenergic stimulation can increase BAT 18F-FDG uptake independently of UCP1 thermogenic function.