The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
Animal models of NASH: Getting both pathology and metabolic context right
Open accessAbstract
Non‐alcoholic fatty liver disease (NAFLD) is the most common cause of referral to liver clinics, and its progressive form, non‐alcoholic steatohepatitis (NASH), can lead to cirrhosis and end‐stage liver disease. The main risk factors for NAFLD/NASH are the metabolic abnormalities commonly observed in metabolic syndrome: insulin resistance, visceral obesity, dyslipidemia and altered adipokine profile. At present, the causes of progression from NAFLD to NASH remain poorly defined, and research in this area has been limited by the availability of suitable animal models of this disease. In the past, the main models used to investigate the pathogenesis of steatohepatitis have either failed to reproduce the full spectrum of liver pathology that characterizes human NASH, or the liver pathology has developed in a metabolic context that is not representative of the human condition. In the last few years, a number of models have been described in which the full spectrum of liver pathology develops in an appropriate metabolic context. In general, the underlying cause of metabolic defects in these models is chronic caloric overconsumption, also known as overnutrition. Overnutrition has been achieved in a number of different ways, including forced feeding, administration of high‐fat diets, the use of genetically hyperphagic animals, or a combination of these approaches. The purpose of the present review is to critique the liver pathology and metabolic abnormalities present in currently available animal models of NASH, with particular focus on models described in approximately the last 5 years.
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Cites
Design and validation of a histological scoring system for nonalcoholic fatty liver disease†
Kleiner, D. E., Brunt, E. M., Van Natta, M., Behling, C., Contos, M. J., Cummings, O. W., Ferrell, L. D., Liu, Y., Torbenson, M. S., Unalp‐Arida, A., et al. (2005) · Hepatology · doi:10.1002/hep.20701 · Cited by 10,791
Self-citationRandle, P. J., Garland, P. B., Hales, C. N., & Newsholme, E. A. (1963) · The Lancet · doi:10.1016/s0140-6736(63)91500-9 · Cited by 5,093
Steatohepatitis: A tale of two “hits”?
Day, C. P., & James, O. F. W. (1998) · Gastroenterology · doi:10.1016/s0016-5085(98)70599-2 · Cited by 4,285
Nonalcoholic fatty liver disease: a spectrum of clinical and pathological severity.
MATTEONI, C., YOUNOSSI, Z., GRAMLICH, T., BOPARAI, N., LIU, Y., & MCCULLOUGH, A. (1999) · Gastroenterology · doi:10.1016/s0016-5085(99)70506-8 · Cited by 3,345
Molecular mediators of hepatic steatosis and liver injury
Browning, J. D., & Horton, J. D. (2004) · Journal of Clinical Investigation · doi:10.1172/jci200422422 · Cited by 1,772
Hypothalamic and genetic obesity in experimental animals: an autonomic and endocrine hypothesis
Bray, G. A., & York, D. A. (1979) · Physiological Reviews · doi:10.1152/physrev.1979.59.3.719 · Cited by 1,132
Beyond insulin resistance in NASH: TNF-α or adiponectin?
Hui, J. M., Hodge, A., Farrell, G. C., Kench, J. G., Kriketos, A., & George, J. (2004) · Hepatology · doi:10.1002/hep.20280 · Cited by 942
JNK1 but not JNK2 promotes the development of steatohepatitis in mice
Schattenberg, J. M., Singh, R., Wang, Y., Lefkowitch, J. H., Rigoli, R. M., Scherer, P. E., & Czaja, M. J. (2006) · Hepatology · doi:10.1002/hep.20999 · Cited by 384
Fan, C.-Y., Pan, J., Usuda, N., Yeldandi, A. V., Rao, M. S., & Reddy, J. K. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.25.15639 · Cited by 343
Sahai, A., Malladi, P., Pan, X., Paul, R., Melin-Aldana, H., Green, R. M., & Whitington, P. F. (2004) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00199.2004 · Cited by 290
Cited by
NLRP3 inflammasome blockade reduces liver inflammation and fibrosis in experimental NASH in mice
Mridha, A. R., Wree, A., Robertson, A. A. B., Yeh, M. M., Johnson, C. D., Van Rooyen, D. M., Haczeyni, F., Teoh, N. C.-H., Savard, C., Ioannou, G. N., et al. (2017) · Journal of Hepatology · doi:10.1016/j.jhep.2017.01.022 · Cited by 1,110
Self-citationThe role of macrophages in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis
Kazankov, K., Jørgensen, S. M. D., Thomsen, K. L., Møller, H. J., Vilstrup, H., George, J., Schuppan, D., & Grønbæk, H. (2019) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-018-0082-x · Cited by 941
Nonalcoholic Fatty Liver Disease: Pathology and Pathogenesis
Tiniakos, D. G., Vos, M. B., & Brunt, E. M. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-121808-102132 · Cited by 870
The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome
Lim, J. S., Mietus-Snyder, M., Valente, A., Schwarz, J.-M., & Lustig, R. H. (2010) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2010.41 · Cited by 771
Animal models of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis
Takahashi, Y. (2012) · World Journal of Gastroenterology · doi:10.3748/wjg.v18.i19.2300 · Cited by 554
Metadata
- Authors
- Larter, C. Z., & Yeh, M. M.
- Venue
- Journal of Gastroenterology and Hepatology
- Publisher
- Wiley
- Published
- 2008-11
- Volume
- 23
- Issue
- 11
- Pages
- 1635-1648
- ISSN
- 0815-9319 (ISSN-L)
- 1440-1746
- OpenAlex
- W2125720510
- Cited by
- 337
- References
- 14
- FWCI
- 15.11
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Larter, C. Z., & Yeh, M. M. (2008). Animal models of NASH: Getting both pathology and metabolic context right. Journal of Gastroenterology and Hepatology. https://doi.org/10.1111/j.1440-1746.2008.05543.x
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
