Hepatic fructose metabolism. Of an ingested sucrose load, 20% of the glucose and 100% of the fructose is metabolized by the liver. Fructose induces the following: 1) substrate-dependent phosphate depletion, which increases uric acid and contributes to hypertension via inhibition of endothelial nitric oxide synthase and reduction of nitric oxide (NO); 2) de novo lipogenesis and dyslipidemia; 3) hepatic lipid droplet formation and steatosis; 4) muscle insulin resistance; 5) c-jun N-terminal kinase (JNK1) activation, contributing to hepatic insulin resistance, which promotes hyperinsulinemia and influences substrate deposition into fat; 6) increased forkhead protein O1 (FoxO1), promoting gluconeogenesis (GNG) and hyperglycemia; and 7) central nervous system hyperinsulinemia, which antagonizes central leptin signaling and promotes continued energy intake. ACC, acetyl CoA carboxylase; ACL, ATP citrate lyase; ACSS2, acyl-CoA synthetase short-chain family member 2; ApoB, apolipoprotein B; ChREBP, carbohydrate response element binding protein; CPT-1, carnitine palmitoyl transferase 1; FAS, fatty acid synthase; Glut2, glucose transporter 2; Glut4, glucose transporter 4; Glut 5, glucose transporter 5; GSK, glycogen synthase kinase; IR, insulin resistance; IRS-1, insulin receptor substrate 1; LPL, lipoprotein lipase; MKK7, MAP kinase kinase 7; MTP, microsomal transfer protein; PFK, phosphofructokinase; PGC-1β, PPAR-γ coactivator-1β PI3K, phosphatidylinositol 3-kinase; PKCɛ, protein kinase C-ɛ PP2A, protein phosphatase 2a; SREBP-1c, sterol regulatory element binding protein 1c. Reproduced from () with permission.