(A) VSG induced a reduction in hematocrit levels that could not be countered by high dietary iron levels. Average ± SEM; sham-regular, n = 13; sham-Fe+, n = 20; VSG-regular, n = 8; VSG-Fe+, n = 12; two-way ANOVA, main effect ####p < 0.0001 surgery effect, multiple comparisons post hoc Tukey test, **p < 0.01, ***p < 0.001.
(B) VSG induced a reduction in circulating iron levels that could not be countered by high dietary iron levels. Two-way ANOVA, main effect ##p < 0.01 surgery effect, multiple comparisons post hoc Tukey test, **p < 0.01.
(C) Circulating hepcidin levels were mostly increased in mice with VSG on a high-iron diet. Two-way ANOVA, main effects σσσP<0.001: dietary iron effect, ###p < 0.001: surgery effect, ΔΔp<0.01: interaction dietary iron*surgery; multiple comparisons post hoc Tukey test, ****p < 0.0001.
(D) VSG surgery, but not HepcidinΔliver, increased total iron binding capacity (TIBC). Average ± SEM; sham-WT, n = 7; VSG-WT, n = 4; sham-HepcidinΔliver, n = 8; VSG-HepcidinΔliver, n = 6; #p < 0.05, two-way ANOVA, main effect of surgery.
(E) HepcidinΔLiver increased circulating iron levels independent of surgery, although an interaction of lower iron levels in WT VSG was observed. Δp<0.05: two-way ANOVA, interaction of genotype*surgery.
(F) At the level of transferrin saturation, a main effect of HepcidinΔLiver, VSG surgery, and an interaction of genotype*surgery were observed. Two-way ANOVA, ****p < 0.0001: main effect of genotype, ###p < 0.001: main effect of surgery, ΔΔp < 0.01: interaction genotype*surgery.