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Volume 134, Issue 2, Pages 622-625 (February 2008)
Endocannabinoids, CB1 Receptors, and Liver Disease: Hitting More Than One Bird With the Same Stone George Kunos, Bin Gao Gastroenterology Volume 134, Issue 2, Pages (February 2008) DOI: /j.gastro Copyright © 2008 AGA Institute Terms and Conditions
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Figure 1 Schematic representation of the hepatic fibrogenic and steatogenic actions of endocannabinoids. Fibrogenic stimuli, such as CCl4 or ethanol, selectively induce 2-AG production in stellate cells.10,30 2-AG can then activate CB1 receptors on stellate cells to induce fibrogenesis,7 or on adjacent hepatocytes to induce de novo lipogenesis.10 Lipogenic stimuli, such as a high-fat diet, induces anandamide (AEA) production and CB1 expression in hepatocytes, activation of which increases de novo lipogenesis and inhibits fatty acid β-oxidation.9Abbreviations: FAAH, fatty acid amidohydrolase; AMPK, AMP-activated protein kinase; SREBP1c, sterol response element binding protein-1c; ACC1, acetyl CoA carboxylase-1; FAS, fatty acid synthase; SCD1, stearoyl CoA desaturase-1; CPT1, carnitine palmitoyl transferase-1. Gastroenterology , DOI: ( /j.gastro ) Copyright © 2008 AGA Institute Terms and Conditions
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