Abstract
NASH is a complex metabolic disease best understood by recognizing the sources and fates of major metabolic substrates (carbohydrates and fatty acids) and how their excess can lead to lipotoxic liver injury with a histological phenotype of NASH. With this perspective, targets of therapy can be predicted. This review summarizes recent clinical trial data and where these trials fit into the substrate overload lipotoxic liver injury paradigm of NASH pathogenesis. Because NASH is likely the result of diverse environmental, genetic, and epigenetic factors that differ among patients, no single therapy is likely to be effective in all patients. Ultimately, rationally designed personalized therapy will be achieved for patients with NASH, but this will require substantial new knowledge on why patients respond to specific therapies, a goal that remains elusive. Hopefully, this gap in knowledge will be addressed by analysis of responders and non-responders in current and future clinical trials.
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