Fig. 1: In utero VD deficiency reprograms HSCs to transfer IR.

A–J Vitamin D-sufficient CD45.1⁺ C57BL6 mice were transplanted with VD(−) or VD( + ) FL-HSCs from CD45.2⁺ C57BL6 mice (primary; n = 20/group), then these primary recipients were used as BM transplant donors for vitamin D-sufficient mice (secondary; 20 transplanted mice/group). Glucose and insulin tolerance tests were performed at (A, B) 8 weeks VD(−)(n = 18, VD( + ) = 20 mice/group from two independent experiments) and C, D 6 months post-primary-transplant (VD(−) n = 15, VD(+) n = 16 mice) and E, F 8 weeks post-secondary-transplant (n = 12/group). The area under the curve is included on the glucose tolerance test insets. Hyperglycemic-euglycemic clamps were conducted in primary transplant recipients after 8 weeks (n = 4/group). Data are reported as G glucose infusion rate, H insulin-stimulated glucose disposal rate (Rd), I change in hepatic glucose production, and J insulin-stimulated 2-DG uptake in adipose tissue. K–M Primary eWAT was isolated from VD(−) or VD( + ) FL-HSC recipients. K Ex vivo insulin-stimulated 2-DG uptake (n = 4/group). L Western blot analysis of phospho- and total AKT levels following insulin stimulation. M Percentage of F4/80-positive cells by manually counting 15 light microscopy fields under ×20 objective per mouse (n = 3/group). Data presented as mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001 vs. VD( + ) FL-HSCs recipients by two-tailed unpaired t test. Actual P values are shown in the source data file.