Review
Copyright ©The Author(s) 2016.
World J Diabetes. Jul 10, 2016; 7(13): 260-270
Published online Jul 10, 2016. doi: 10.4239/wjd.v7.i13.260
Figure 5
Figure 5 Conflicting mechanisms of metabolic regulation via intestinal farnesoid X receptor activity. A: FXR activation decreases hepatic TG levels and improves glucose metabolism; B: Intestinal FXR activation of FXR agonist leads to FGF-15/19 production and improves nonalcoholic fatty liver disease. Synthesized FGF-15/19 changes BA metabolism and serum BA composition, which causes TGR5/M-BAR activation, reduced inflammatory cytokine release, and improved insulin resistance. BABR: Bile acid binding resin; FGF-15/19: Fibroblast growth factor-15/19; FXR: Farnesoid X receptor; NAFLD: Nonalcoholic fatty liver disease; SREBP1c: Sterol regulatory element-binding protein 1c; Tβ-MCA: Tauro-β-muricholic acid; GLP-1: Glucagon-like peptide-1; TG: Triglyceride.