A pilot study of pioglitazone treatment for nonalcoholic steatohepatitis
By K. Promrat, G. Lutchman, G. Uwaifo, Renee J. Freedman, A. Soza, T. Heller, E. Doo, M. Ghany, A. Premkumar, Y. Park and 4 more. Hepatology, 2004
735 citations recorded by the source corpus.
Subfields: Epidemiology, Surgery
View Paper: https://www.semanticscholar.org/paper/90426913059d50b66252bba9648512ab0bd3355c
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Citations in the corpus
- Long-Term Pioglitazone Treatment for Patients With Nonalcoholic Steatohepatitis and Prediabetes or Type 2 Diabetes Mellitus (2016, neutral): “001 Aspartate aminotransferase level, U/L 38 (31) 29 (10) −14 (−22 to −6) 0.”
- Local and systemic insulin resistance resulting from hepatic activation of IKK-β and NF-κB (2005, methodology): “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.”
- Molecular mediators of hepatic steatosis and liver injury. (2004, positive): “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.”
- Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease. (2005, background): “Indeed, NAFLD patients treated with insulin-sensitizing agents show marked improvement in their condition (28, 30, 31).”
- A Randomized Controlled Trial of Metformin versus Vitamin E or Prescriptive Diet in Nonalcoholic Fatty Liver Disease (2005, methodology): “However, the use of use of enzyme levels as surrogate markers is supported by the association of higher aminotransferases with more severe histological findings in cross-sectional studies (4), and by the finding that reduced aminotransferases are associated with improved histology in intervention st”