Improved nonalcoholic steatohepatitis after 48 weeks of treatment with the PPAR‐γ ligand rosiglitazone

By B. Neuschwander‐Tetri, E. Brunt, K. Wehmeier, D. Oliver, B. Bacon. Hepatology, 2003

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Local and systemic insulin resistance resulting from hepatic activation of IKK-β and NF-κB (2005, neutral): “We isolated IKK complexes from mouse liver lysates using anti-IKK-γ antibodies (PharMingen) coupled to protein A-Sepharose, and conducted in vitro kinase assays at 30 °C by adding [γ-32P]ATP and 2 μg of GST-IκBα (1-54)12.”
ENDPOINTS AND CLINICAL TRIAL DESIGN FOR NONALCOHOLIC STEATOHEPATITIS (2011, background): “Several clinical trials have shown that reversal of steatohepatitis and the individual features of steatohepatitis can improve as early as 6-12 months.(36,37) Fibrosis progresses slowly over years; conversely, it is generally believed that clinically significant improvement in fibrosis also takes lo”
Magnetic resonance spectroscopy to measure hepatic triglyceride content: prevalence of hepatic steatosis in the general population. (2005, background): “For patients with diabetes, rosiglitazone treatment results in a 40% reduction in plasma free fatty acid levels and hepatic triglyceride content (HTGC), which is accompanied by a marked improvement in insulin-stimulated glucose metabolism during insulin clamp studies (29, 31).”
Molecular mediators of hepatic steatosis and liver injury. (2004, neutral): “Pilot studies in humans using pioglitazone (57, 58) and rosiglitazone (59) have demonstrated the efficacy of these agents in reducing hepatic fat, presumably as a consequence of the molecular events summarized in Figure 2.”