Primary bile acids (BAs) are produced by hepatocytes as the products of cholesterol catabolism. They are vital for the intestinal absorption of lipophilic nutrients and the hepatobiliary secretion of endogenous and xenobiotic metabolites. They also act as signalling molecules and play important roles in the regulation of glucose lipid metabolism in the enterohepatic system and peripheral tissues (Chiang, 2009; Li and Chiang, 2012). Given their essentiality for health, but toxicity at high levels, it is not surprising that BA synthesis is tightly regulated.
Here we provide the model of bile acid homeostasis in human hepatocytes used in our publication (Bioinformatics 2013; doi: 10.1093/bioinformatics/btt552) to demonstrate power of our approach in dynamic simulation of molecular interaction networks involving gene regulation, signalling and whole-cell metabolism in human cells. We created a model of gene regulatory and signalling network (206 Petri Net places, 214 Petri Net transitions) regulating 269 metabolic reactions (11%) in whole-cell metabolic model of human hepatocyte (HepatoNet1).
The HepatocyteQSSPN.zip file (Download link) contains model distribution. See README.pdf file in software distribution for content description. The HepatocyteQSSPN.pdf (Network overview link) file contains network map giving overview of the scope of our model.