Editorial
Copyright ©2011 Baishideng Publishing Group Co.
World J Gastroenterol. Sep 28, 2011; 17(36): 4055-4062
Published online Sep 28, 2011. doi: 10.3748/wjg.v17.i36.4055
Figure 1
Open in New Tab Full Size Figure Download Figure
Figure 1 Underlying mechanisms of the complex interaction resulting in steatosis in patients with hepatitis C virus. HCV: Hepatitis C virus.
Figure 2
Open in New Tab Full Size Figure Download Figure
Figure 2 Cross-talk among the insulin sensitive organs.
Figure 3
Open in New Tab Full Size Figure Download Figure
Figure 3 Insulin signaling pathways. PI3-K: Phosphatidyl inositol 3-kinase; AkT: A serine/threonine protein kinase.
Figure 4
Open in New Tab Full Size Figure Download Figure
Figure 4 Pathways to insulin resistance. PKC: Protein kinase C; IKK: Inhibitor κB kinase; TNF: Tumor necrosis factor; NF: Nuclear factor; SOCS: Suppressors of cytokine signaling; IRS: Insulin receptor substrate.
Figure 5
Open in New Tab Full Size Figure Download Figure
Figure 5 Insulin resistance and cell death. FFA: Free fatty acids; TGL: Tryglycerides.
Figure 6
Open in New Tab Full Size Figure Download Figure
Figure 6 Fate of accumulated fat within hepatocytes.