The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Dietary fructose in nonalcoholic fatty liver disease
Open accessAbstract
Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in adults and children. A number of genetic and environmental factors are known to predispose individuals to NAFLD. Certain dietary sugars, particularly fructose, are suspected to contribute to the development of NAFLD and its progression. The increasing quantity of fructose in the diet comes from sugar additives (most commonly sucrose and high fructose corn syrup) in beverages and processed foods. Substantial links have been demonstrated between increased fructose consumption and obesity, dyslipidemia, and insulin resistance. Growing evidence suggests that fructose contributes to the development and severity of NAFLD. In human studies, fructose is associated with increasing hepatic fat, inflammation, and possibly fibrosis. Whether fructose alone can cause NAFLD or if it serves only as a contributor when consumed excessively in the setting of insulin resistance, positive energy balance, and sedentary lifestyle is unknown. Sufficient evidence exists to support clinical recommendations that fructose intake be limited through decreasing foods and drinks high in added (fructose-containing) sugars.
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Risk of Cardiovascular Disease in Patients with Nonalcoholic Fatty Liver Disease
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“5% of calories from fructose).(69) We far exceed that level today.”
BackgroundHavel, P. J. (2005) · Nutrition Reviews · doi:10.1111/j.1753-4887.2005.tb00132.x · Cited by 607
Maersk, M., Belza, A., Stødkilde-Jørgensen, H., Ringgaard, S., Chabanova, E., Thomsen, H., Pedersen, S. B., Astrup, A., & Richelsen, B. (2012) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.111.022533 · Cited by 603
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“In this study, PNPLA3 genotype did not affect hepatic or visceral fat gain.(66) Fructose Avoidance May Improve NAFLD.”
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Cited by
Treatment of NAFLD with diet, physical activity and exercise
Romero-Gómez, M., Zelber-Sagi, S., & Trenell, M. (2017) · Journal of Hepatology · doi:10.1016/j.jhep.2017.05.016 · Cited by 1,347
Hepatic inflammation and fibrosis: Functional links and key pathways
Seki, E., & Schwabe, R. F. (2015) · Hepatology · doi:10.1002/hep.27332 · Cited by 972
Fructose stimulated de novo lipogenesis is promoted by inflammation
Todoric, J., Di Caro, G., Reibe, S., Henstridge, D. C., Green, C. R., Vrbanac, A., Ceteci, F., Conche, C., McNulty, R., Shalapour, S., et al. (2020) · Nature Metabolism · doi:10.1038/s42255-020-0261-2 · Cited by 328
Food, immunity, and the microbiome
Tilg, H., & Moschen, A. R. (2015) · Gastroenterology · doi:10.1053/j.gastro.2014.12.036 · Cited by 292
Non-alcoholic fatty liver and the gut microbiota
Bashiardes, S., Shapiro, H., Rozin, S., Shibolet, O., & Elinav, E. (2016) · Molecular Metabolism · doi:10.1016/j.molmet.2016.06.003 · Cited by 241
Metadata
- Authors
- Vos, M. B., & Lavine, J. E.
- Venue
- Hepatology
- Published
- 2013-06
- Volume
- 57
- Issue
- 6
- Pages
- 2525-2531
- ISSN
- 0270-9139 (ISSN-L)
- OpenAlex
- W2058383228
- Cited by
- 314
- References
- 8
- FWCI
- 22.17
- Type
- journal article
- Language
- en
- Open access
- bronze
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
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.
