Cristoforo Silvestri, Vincenzo Di Marzo Cell Metabolism

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The Endocannabinoid System in Energy Homeostasis and the Etiopathology of Metabolic Disorders Cristoforo Silvestri, Vincenzo Di Marzo Cell Metabolism Volume 17, Issue 4, Pages 475-490 (April 2013) DOI: 10.1016/j.cmet.2013.03.001 Copyright © 2013 Elsevier Inc. Terms and Conditions

Figure 1 Endocannabinoid- and CB1-Mediated Control of Central Functions Affecting Food Intake and Metabolism 2-AG, 2-arachidonoylglycerol; BAT, brown adipose tissue; CRH, corticotrophin-releasing hormone; EC, endocannabinoid; glut., glutamate; MCH, melanin-concentrating hormone. Cell Metabolism 2013 17, 475-490DOI: (10.1016/j.cmet.2013.03.001) Copyright © 2013 Elsevier Inc. Terms and Conditions

Figure 2 Endocannabinoid Function in the Adipose Tissue AEA, anandamide; BAT, brown adipose tissue; EC, endocannabinoid; FA, fatty acid; FAS, fatty acid synthase; LPL, lipoprotein lipase; PPARγ, peroxisome proliferator-activated receptor-γ; TG, triglyceride. Cell Metabolism 2013 17, 475-490DOI: (10.1016/j.cmet.2013.03.001) Copyright © 2013 Elsevier Inc. Terms and Conditions

Figure 3 Endocannabinoid Role in Lipid and Glucose Metabolism in the Liver Endocannabinoid control of hepatocyte (A) triglyceride levels and (B) insulin sensitivity and glucose production. In (B), note how hepatocyte CB1 activation has been proposed to inhibit insulin signaling by two mechanisms, i.e., upregulation of inhibitory phosphorylation of insulin receptor substrate (IRS) and stimulation of inhibitory dephosphorylation of insulin-activated protein kinase b (AKT2) via the upregulation of the S/T phosphatase PH domain and leucine-rich repeat protein phosphatase 1 (PHLPP11) downstream of a pathway dependent on heat shock protein 5 (HSPA5), PRKR-like endoplasmic reticulum kinase (PERK) and eukaryotic translation initiation factor 2 subunit 1 alpha (eIF2α) and subsequent endoplasmic reticulum (ER) stress (Liu et al., 2012). CB1-activated ER stress is also implicated in the upregulation of the liver-specific transcription factor cAMP-responsive element-binding protein H (CREBH), which increases gluconeogenic gene expression and glucose production via Lipin1 and potential feed-forward onto endocannabinoid (EC) biosynthesis (Chanda et al., 2011). ACACA, acetyl-Coenzyme A carboxylase-α; CPT1a, carnitine palmitoyltransferase 1a; CREBH, cAMP-responsive element-binding protein H; DAG, diacyl glycerol; FA, fatty acid; FAS, fatty acid synthase; HFD, high-fat diet; HSC, hepatic stellate cell; IDE, insulin-degrading enzyme; IR, insulin receptor; LKB1, liver kinase B1; LXRa, liver X receptor a; PKA, cAMP-dependent protein kinase A; PKCε, protein kinase Cε; RAR, retinoic acid receptor; SREBF1, sterol regulatory element binding factor 1. Cell Metabolism 2013 17, 475-490DOI: (10.1016/j.cmet.2013.03.001) Copyright © 2013 Elsevier Inc. Terms and Conditions