Mutant JAK2–induced MPNs were vulnerable to modulation of nutrients in vivo. (A) Mice were induced by tamoxifen and treated with normal diet (ND) or HGD for 7 weeks. Time course of nonfasting blood glucose levels (n = 5-6 mice per treatment and genotype). (B) Peripheral blood counts of HGD- and ND-treated mice (n = 5-6 mice per genotype). (C) Spleen weight after 7 weeks of ND or HGD (n = 5-6 mice per treatment and genotype). (D) Nonfasting blood glucose levels in mice exposed to fed-fasting cycles or continuously fed with ND (n = 4-5 mice per genotype and condition). (E) Peripheral blood counts of mice exposed to fed-fasting cycles or continuously fed with ND. (F) Spleen weight in mice exposed to fed-fasting cycles or ND (n = 4-5 mice per genotype and condition). (G) Correlation of nonfasting blood glucose levels with peripheral blood counts. Peripheral blood counts and nonfasting blood glucose levels were monitored 6 to 8 weeks after tamoxifen injections (n = 4-5 mice per genotype). (H-I) Glucose uptake capacity of erythroid cells in spleen monitored by 2-NBDG fluorescence. After 4 hours of starvation, cells from spleen or BM were exposed to 2-NBDG for 30 minutes and analyzed by flow cytometry. (H) Histograms show 2-NBDG fluorescence in splenic CD71⁺Ter119⁺ cells, with quantification of the mean fluorescence intensity (MFI) presented as bar graphs (middle). 2-NBDG MFI in subsets of erythroid cells (I-V) (right). (I) Glucose uptake capacity of erythroid cells in bone marrow (n = 6 mice per genotype). All data are presented as mean ± standard error of the mean. One- or 2-way analyses of variance followed by Tukey’s multiple comparison tests were used for multiple-group comparisons. *P < .05, **P < .01. RBC, red blood cell.