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
Published online Jul 10, 2016. doi: 10.4239/wjd.v7.i13.260
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.
- Citation: Taoka H, Yokoyama Y, Morimoto K, Kitamura N, Tanigaki T, Takashina Y, Tsubota K, Watanabe M. Role of bile acids in the regulation of the metabolic pathways. World J Diabetes 2016; 7(13): 260-270
- URL: https://www.wjgnet.com/1948-9358/full/v7/i13/260.htm
- DOI: https://dx.doi.org/10.4239/wjd.v7.i13.260