Fig. 3: [¹⁸F]F-AraG accumulates in adrenergically stimulated brown and bone marrow adipocytes.

a Chronic adrenergic stimulation of thermogenesis-deficient Letmd1-KO mice did not result in increased [¹⁸F]F-AraG uptake in either iBAT or BMAT. b BRL37344 treatment did not lead to a significant increase in [¹⁸F]F-AraG accumulation in the iBAT (p = 0.08) or lumbar BMAT (p = 0.14). Signal in the cervical vertebrae increased marginally (12.5%) post adrenergic stimulation (p = 0.02). c There was no increase in the abundance of adipocyte or lymphocyte in the femoral bone marrow of adrenergically stimulated Letmd1 KO mice. Frequency of the subset is shown. d In Letmd1-KO mice, the adipocyte population in the femoral bone marrow constituted the majority of cells with a high mitochondrial content. BRL37344 did not change mitochondrial content of femur bone marrow adipocytes. e In femur bone marrow, adrenergic stimulation of Letmd1-KO mice decreased the population of adipocytes rich in mitochondria. f In T cell-deficient Rag1-KO mice, treatment with BRL37344 resulted in increased accumulation of [¹⁸F]F-AraG in iBAT, whereas there was no notable change in BMAT. g After adrenergic stimulation, [¹⁸F]F-AraG signal in the iBAT increased by close to threefold (p = 0.002), while the signal in BMAT did not show significant changes. h The frequency of adipocytes in the bone marrow of Rag1-KO mice increased significantly post adrenergic stimulation (p = 0.01). Frequency of the subset is depicted. i. Rag1 deficiency reduced mitochondrial content in femur bone marrow adipocytes. j The proportion of mitochondria-rich bone marrow adipocytes remained unchanged in adrenergically stimulated Rag1-KO mice (p = 0.75). k In wt mice, ¹⁸FDG accumulated in the adrenergically stimulated iBAT but not in the BMAT. Data are shown as mean ± SD (n = 5). Each spot represents an individual mouse. * p ≤ 0.05; ** p ≤ 0.01; *** p ≤ 0.001; **** p < 0.0001.