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. 2020 Jun 5;11:2847. doi: 10.1038/s41467-020-16662-2

Fig. 3. GCN2 deletion in amygdala markedly blunts leucine deprivation-induced WAT browning.

Fig. 3

a P-GCN2, t-GCN2, p-eIF2α, and t-eIF2α proteins in amygdala by western blotting (left) and quantified by densitometric analysis (right); A.U.: arbitrary units. b Daily food intake. c Fat mass by NMR. d Subcutaneous WAT (sWAT) weight. e Representative images of hematoxylin and eosin (H&E) staining of sWAT. f sWAT cell size quantified by Image J analysis of H&E images. g Gene expression of Ucp1, Pgc1a, Cidea, Dio2, and Prdm16 in sWAT by RT-PCR. h Representative images of immunohistochemistry (IHC) staining of UCP1 in sWAT. i UCP1 protein in sWAT by western blotting (left) and quantified by densitometric analysis (right). All studies were conducted using 20- to 22-week-old male control mice (GCN2+/+) or mice with GCN2 deletion in amygdala (GCN2 KO) fed a control (Control) or leucine-deficient [(-) L] diet for 3 days. Data are expressed as the mean ± SEM (n represents number of samples and are indicated above the bar graph), with individual data points. Data were analyzed by two-tailed unpaired Student’s t test for (a), or by one-way ANOVA followed by the SNK (Student–Newman–Keuls) test for (b–i). Source data are provided as a Source data file.