Metformin reverses fatty liver disease in obese, leptin-deficient mice

By Huizhi Lin, Shiqi Yang, Christine Chuckaree, F. Kuhajda, Gabriele Ronnet, A. Diehl. Nature Medicine, 2000

700 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f7886e69cbf64f194351ce82ff64bb407f55c728

How researchers see this paper

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

In Endocrinology, Diabetes and Metabolism

1. Herbert Tilg
2. Bruce E. Kemp
3. J. Lo
4. E. Bugianesi
5. G. Steinberg
6. A. Moschen
7. Michael Pollak
8. D. Hardie

In Epidemiology

1. Herbert Tilg
2. Giulio Marchesini
3. A. Moschen
4. A. McCullough
5. D. Moller
6. Bruce E. Kemp
7. E. Bugianesi
8. G. Steinberg

In Molecular Biology

1. G. Steinberg
2. Michael Pollak
3. D. Hardie
4. B. Viollet
5. D. Moller
6. Kathleen M. Giacomini
7. Bruce E. Kemp
8. Herbert Tilg

Citations in the corpus

• Molecular mediators of hepatic steatosis and liver injury. (2004, unknown): “Treatment of ob/ob mice with metformin markedly reduced hepatic steatosis (53), and its administration to humans with NASH improved LFT numbers and decreased liver size (54).”
• Nonalcoholic fatty liver disease: a feature of the metabolic syndrome. (2001, background): “Such a hypothesis has been recently tested in an animal model (55).”
• Role of AMP-activated protein kinase in mechanism of metformin action. (2001, background): “Metformin also decreases hepatic lipids in obese mice (9).”
• AMPK in Health and Disease. (2009, background): “Interestingly, metformin also reduces inflammatory markers such as TNF- (294) and C-reactive protein (179), effects that are likely mediated by AMPK inhibition of NF B transcription (71), suggesting a secondary mechanism by which AMPK may improve insulin sensitivity.”
• Cellular and molecular mechanisms of metformin: an overview. (2012, background): “Evidence that metformin improved fatty liver disease by reversing hepatic steatosis in ob/ob mice [48, 49] and in rodents fed a high-fat diet [50] has been demonstrated but also reported in some clinical studies [51, 52].”
• Effect of genetic variation in the organic cation transporter 1 (OCT1) on metformin action. (2007, background): “In addition, the drug has recently been implicated in the treatment and/or prevention of fatty liver diseases and polycystic ovary syndrome (2, 3).”
• Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis (2010, background): “Anti-TNF antibody treatment and metformin, an antidiabetic drug that inhibits hepatic TNFa expression, improve steatosis in ob/ob mice.(23,24) Other proinflammatory mediators might also contribute to the development of steatosis because in some studies hepatic steatosis was not dependent on TNFa.”