Have guidelines addressing physical activity been established in nonalcoholic fatty liver disease?

Figure 2 Mechanisms for free fatty acid-induced skeletal muscle insulin resistance. A: Normal glucose uptake into skeletal muscle occurs via binding of insulin to the insulin receptor, resulting in receptor autophosphorylation and subsequent binding and tyrosine phosphorylation of insulin receptor substrate (IRS)-1. Subsequently, phosphatidylinositol 3-kinase (PI3K) is activated and results in downstream activation of protein kinase B, leading to glucose transporter (GLUT)-4 translocation to the myocyte plasma membrane and glucose uptake into the cell; B: Increased intramyocellular lipid content leads to the activation of protein kinase Ch (PKCh) which results in serine phosphorylation of IRS-1, thereby inhibiting its tyrosine phosphorylation. This prevents the activation of PI3K and GLUT-4 translocation to the cell surface. Thus glucose entry into the cell is inhibited. AMPK: AMP-activated protein kinase; DAG: Diacylglycerol; FFA: Free fatty acid; Akt: Protein Kinase B.