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. 2013 Mar 6;4(2):226–235. doi: 10.3945/an.112.002998

Figure 1.

Figure 1

Hepatic glucose metabolism. Of an ingested glucose load, 20% is metabolized by the liver. Under the action of insulin, glycogen synthase is increased, and the majority of the glucose load is stored as glycogen. Although insulin activation of sterol response element binding protein 1c (SREBP-1c) activates the lipogenic pathway, there is little citrate formed to act as a substrate for lipogenesis. In addition, insulin action on the liver phosphorylates forkhead protein O1 (FoxO1), excluding it from the nucleus, and suppressing the enzymes involved in gluconeogenesis (GNG). 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; IRS-1, insulin receptor substrate 1; MTP, microsomal transfer protein; PFK, phosphofructokinase; PI3K, phosphatidylinositol 3-kinase; SREBP-1c, sterol regulatory element binding protein 1c. Reproduced from (59) with permission.