Hepatic lipotoxicity and the pathogenesis of nonalcoholic steatohepatitis: The central role of nontriglyceride fatty acid metabolites

By B. Neuschwander‐Tetri. Hepatology, 2010

1,037 citations recorded by the source corpus.

Subfields: Biochemistry, Endocrinology, Diabetes and Metabolism, Epidemiology

View Paper: https://www.semanticscholar.org/paper/108fad8d6d56bebfe04a8166058c96e397ca2b0e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Biochemistry

1. M. Pinzani
2. K. Cusi
3. G. Hotamışlıgil

In Endocrinology, Diabetes and Metabolism

1. Z. Younossi
2. K. Cusi
3. A. Sanyal
4. M. Pinzani
5. E. Tsochatzis
6. E. Buzzetti
7. G. Hotamışlıgil
8. Haiming Cao

In Epidemiology

1. Z. Younossi
2. A. Sanyal
3. K. Cusi
4. E. Brunt
5. J. Lavine
6. A. Diehl
7. N. Chalasani
8. Ali Canbay

Citations in the corpus

• The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, background): “[22] Neuschwander-Tetri BA.”
• The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology. (2012, background): “**The Adult Treatment Panel III clinical definition of the metabolic syndrome requires the presence of three or more of the following features: (1) waist circumference greater than 102 cm in men or greater than 88 cm in women; (2) triglyceride level 150 mg/dL or greater; (3) high-density lipoprotein”
• Long-Term Pioglitazone Treatment for Patients With Nonalcoholic Steatohepatitis and Prediabetes or Type 2 Diabetes Mellitus (2016, neutral): “001 Fibrosis ≥1-point improvement, n (%) 13 (25) 20 (39) 14 (−6 to 34) 0.”
• The interaction of hepatic lipid and glucose metabolism in liver diseases. (2012, background): “The long-lasting paradigm claiming TAG accumulation to be the ‘‘first hit‘‘ that predisposes to further liver damage in the pathogenesis of NASH has recently been replaced by a more complex model as emerging evidence points to FAs and their metabolites as the true lipotoxic agents [7].”
• Trends in insulin resistance: insights into mechanisms and therapeutic strategy (2022, background): “Patients with MAFLD have increased levels of FFAs owing to a failure of insulin-mediated suppression of lipolysis, and excess FFAs excretion into the bloodstream.(314) In addition to the influence of abnormalities on lipid metabolism, IR also indirectly contributes to MAFLD through inflammation.”
• NLRP3 inflammasome blockade reduces liver inflammation and fibrosis in experimental NASH in mice (2017, background): “The most compelling concept is that hepatocyte injury results from lipotoxicity, a consequence of accumulated toxic lipid species [6,7].”