Fig. 2
From: Fructose contributes to the Warburg effect for cancer growth
Glucose and fructose metabolism for cancer growth. Uric acid blocks aconitase, resulting in the disconnection of fructose metabolism from mitochondrial respiration. Uric acid is a byproduct of fructose metabolism and inhibits aconitase. As a result, fructose metabolism is disconnected from mitochondrial oxidative phosphorylation (OXPHOS), but maintains other metabolic pathways for pentose phosphate pathway (PPP), lactose production, ATP production, and lipid synthesis, all of which likely contributes to the cancer growth. Fructose 1 phosphate (Fru1P) competitively activates GK by releasing from glucokinase regulatory protein (GKRP), accounting for fructose facilitation of glucose utilization. AR, aldose reductase; FK, fructokinase; AldoB, aldolase B; AMPD, AMP deaminase; TK, triokinase