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. Author manuscript; available in PMC: 2021 Jun 24.
Published in final edited form as: Nat Metab. 2020 Sep 17;2(9):974–988. doi: 10.1038/s42255-020-00273-8

Fig. 5 |. Lack of Fgr in BM-derived cells protects from HFD-induced liver steatosis.

Fig. 5 |

a, Schematic indicating the strategy for BM transplantation and HFD treatment, and representative histogram showing full reconstitution of CD45.1 host with CD45.2 donor BM. b, Weight gain over time in HFD-fed mice after BM transplantation of the indicated genotypes (n = 16). c, GTT of BM-transplanted mice as indicated in HFD (n = 9). d, Basal insulin levels in BM-transplanted mice as indicated for the HFD group (n = 10). e, Representative ORO staining of OCT liver sections of the indicated genotypes in HFD. Scale bars: 1 mm (low magnification view) and 100 μm (insets). Quantification of ORO-positive stained area versus total liver area in OCT liver sections of the indicated genotypes in the HFD group (n = 8, right bottom). f, Spectrophotometric enzymatic activities of CS (upper), SCHA versus CS (middle) and ISDH versus CS (bottom) in the different mouse genotypes in the HFD group (n = 8). g, Analysis of leptin levels in the serum of BM-transplanted mice as indicated in the HFD group (n ≥ 6). h, Analysis of ketone bodies (KB) in the urine of BM-transplanted mice as indicated in the HFD group (n ≥ 7). Significance was assessed by linear regression in b and one-way ANOVA with Sidak’s correction for multiple comparisons in d–h. *, P < 0.05; ***, P < 0.001; and ****, P < 0.0001. Each point represents a biological replicate. Data are shown as the mean ± s.e.m.