Fig 1: Changes in circulating metabolite profiles induced by blue light exposure to scWAT.a–d Principal components analysis (PCA) plot (a), metabolite set enrichment analysis (MSEA) of altered pathways in circulation in blue lighted groups compared with non-lightened group (b) or red lightened group (c), and variable importance in projection (VIP) (d) from metabolomics analysis of plasma from 12-15-week-old C57BL/6 J male mice exposed to scWAT by different light wavelengths for 8 days (NO light: n = 7, RED light: n = 6, and BLUE light: n = 6). The colored boxes on the right (d) indicate the relative concentrations of the corresponding metabolite in each group under study. e The relative abundance of circulating histidine and carnosine within the histidine metabolism pathway, employing metabolomics analysis (NO light: n = 7, RED light: n = 6, and BLUE light: n = 6). (f and g) Circulating histidine levels in C57BL/6 J male mice (NO light: n = 6, RED light: n = 6, and BLUE light: n = 6) (f) and Opn3-GKO male mice (NO light: n = 5, and BLUE light: n = 4) (g) with/without light treatment for 8 days, measured by ELISA. h and i Clustered heatmap from metabolomics analysis (h) and the relative abundance of histidine and carnosine (i) in treated scWAT with 8 days of blue light exposure relative to no light, employing metabolomics analysis (NO light: n = 6, and BLUE light: n = 5). (j) A positive correlation between the relative abundance of circulating histidine and the histidine in treated scWAT (n = 11). k–m Relative mRNA expression of histidine metabolism genes, Hdc and Carns1, in treated scWAT (n = 8 per group) (k), murine white adipocytes (n = 4 per condition, three biological replicates) (l), and human white adipocytes (n = 3 per condition, three biological replicates) (m) exposed to 8 days of blue light relative to dark condition. Statistics were performed by MSEA (b and c), VIP score (d) using MetaboAnalyst, two-tailed unpaired Student’s t-tests (g, i, and k–m), one-way ANOVA followed by Tukey’s post hoc test (e and f), and Spearman’s Rank correlation test (two-tailed) (j). n.s. indicates no significant difference. n.d. indicates no determined. Data are represented as mean ± SEM.
Fig 2: Blue light-induced histidine increases HDC-responsive neurons in the hypothalamus and activates BAT via sympathetic nervous system.a Schematic of histidine metabolism pathway showing circulating histidine and FMH (HDC antagonist) mediates histaminergic neurons in the hypothalamus and regulates BAT thermogenesis via sympathetic nervous system (SNS). b Histidine decarboxylase (HDC) activity, normalized to total protein (right panel) or tissue weight (left panel), in the isolated brain tissues containing the hypothalamus in mice treated with/without 8 days of blue light exposure plus PBS or FMH injection. (NO light + PBS: n = 6, BLUE light + PBS: n = 3, and BLUE light + FMH: n = 4). c Immunostaining of histaminergic neurons in the hypothalamus in mice treated with/without 8 days of blue light exposure plus PBS or FMH injection. Sections at 1.7 mm and 2.7 mm posterior to the bregma were stained for mouse HDC (red). DAPI (4′,6-diamidino-2-phenylindole) was used to visualize nuclei (blue). Scale bar: 200 μm (two left columns), 20 μm (three right columns). d Relative tyrosine hydroxylase (Th) mRNA expression in BAT in mice treated with non- or 8 days of blue light exposure to scWAT plus PBS or FMH injection (NO light + PBS: n = 5, BLUE light + PBS: n = 6, and BLUE light + FMH: n = 6). e Th immunostaining (green) in BAT sections from mice treated with/without 8 days blue lighting plus PBS or FMH injection. DAPI (4′,6-diamidino-2-phenylindole) was used to visualize nuclei (blue). Scale bar: 50 μm. f Quantification of percentage Th density in BAT sections (NO light + PBS: n = 5, BLUE light + PBS: n = 5, and BLUE light + FMH: n = 3). Statistics were performed by one-way ANOVA followed by Tukey’s post hoc test. Data are represented as mean ± SEM.
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