Recent advances in network biology have assisted in unraveling the complex pathophysiological processes underlying nonalcoholic fatty liver disease (NAFLD) and its progression to nonalcoholic steatohepatitis (NASH) and cirrhosis1
The close inter-connectivity of the contributory molecular pathways suggests that effective pharmacotherapy may require a coordinated multitargeted approach
Per this premise, endogenous metabolic modulators (EMMs) have emerged as a core class of signaling agents and metabolic substrates with the potential to simultaneously impact multiple metabolic and fibroinflammatory pathways in NASH1
EMMs consisting of amino acids are intrinsically fundamental to core NASH pathways2