Extended Data Fig. 2: Fructose effects on DNL and lipogenic enzymes.
From: Fructose stimulated de novo lipogenesis is promoted by inflammation
a, Cytosolic acetyl-CoA concentrations in 6-month-old CSD and HFrD fed MUP - uPA male mice (n = 9 per CSD group, n=7 per HFrD group). b, Expression of genes encoding FA-oxidizing enzymes in CSD- or HFrD- fed (5 months) MUP-uPA (n=7 per group) and DEN-challenged BL6 male mice (n = 9 per group). c, A metabolic chart comparing pathways through which glucose and fructose are converted to acetyl-CoA in the cytoplasm. GK-glucokinase; KHK-ketohexokinase; GI-glucose isomerase; PFK-phosphofructokinase. Cytoplasmic acetyl-CoA is converted to malonyl-CoA by acetyl-CoA carboxylase (ACC) and malonyl- CoA serves as the building block for synthesis of C16:0 (palmitate) and C18:0 (stearate) by fatty acid synthase (FAS). Expression of ACC1 and FAS is strongly upregulated by prolonged HFrD feeding. d, e, Measurement of newly synthesized FA in livers (d) and jejunum (e) of MUP-uPA male mice using D2O as a tracer after a short-term feeding period (48 hours; n = 7 per group). f, Amounts of F1P in liver and jejunum expressed in arbitrary units (48 hours feeding; n = 7 per group). g, h, Expression of inflammatory and lipogenic genes and ACC1 protein in livers (g) and fecal albumin and serum FITC-dextran concentrations (h) in CSD- or HFrD-fed (48 hours) male mice (n = 7 per group). Unpaired two-sided Student’s t test was used in panels a, b and d-h. Mean ± SEM, *P < 0.05, **P < 0.01. Benjamini-Hochberg FDR adjustment for P-values has been performed on data presented in panels b and g.
