Figure 3. The role of glycogen status on hepatic de novo lipogenesis and VLDL export.

The traffic light system demonstrates flux through a given pathway, where red (thickest lines in black and white version) represents high flux, orange (medium thickness lines in black and white version) represents medium flux, and green (thinnest lines in black and white version) represents low flux. A, low hepatic glycogen status enables ingested fructose to stimulate hepatic glycogen synthesis, allowing flux through lipogenic pathways to remain low. B, high hepatic glycogen status determines that ingested fructose is shunted away from glycogen synthesis and towards lipogenic pathways, which leads to greater VLDL export. G‐6‐P, glucose‐6‐phosphate; G‐1‐P, glucose‐1‐phosphate; UDP, uridine diphosphate glucose; F‐1‐P, fructose‐1‐phosphate; F‐6‐P, fructose‐6‐phosphate; F‐1,6‐P₂, fructose‐1,6‐bisphosphate; Glyc‐3‐P, glyceraldehyde‐3‐phosphate; 1,3‐P₂‐glycerate, 1,3‐bisphosphoglycerate; G‐3‐P, glycerol‐3‐phosphate; 3‐Pgly, 3‐phosphoglycerate; 2‐Pgly, 2‐phosphoglycerate; Acetyl‐CoA, acetyl coenzyme A; Malonyl‐CoA, malonyl coenzyme A; DHAP, dihydroxyacetone phosphate; VLDL, very‐low‐density lipoprotein.