The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Non-alcoholic fatty liver disease
Abstract
Non-alcoholic fatty liver disease (NAFLD) refers to the accumulation of hepatic steatosis not due to excess alcohol consumption. The prevalence of NAFLD is up to 30% in developed countries and nearly 10% in developing nations, making NAFLD the most common liver condition in the world. The pathogenesis of NAFLD is related to insulin resistance and, thus, it is frequently found in individuals who have central obesity or diabetes. Insulin resistance and excess adiposity are associated with increased lipid influx into the liver and increased de novo hepatic lipogenesis, promoting hepatic triglyceride accumulation. Defects in lipid utilization via mitochondrial oxidation and lipid export may also contribute to hepatic lipid build-up. Adipocytokine alterations, lipotoxicity from saturated fatty acids and fructose have been all been implicated in causing hepatocyte injury in NAFLD through pathways involving oxidative and endoplasmic reticulum stress. Clinically, NAFLD is commonly asymptomatic and frequently detected incidentally by blood liver function tests or imaging performed for other reasons. Subjects with NAFLD have a higher mortality rate than the general population and are at increased risk of developing cardiovascular disease and diabetes in the future. Histologically, NAFLD occurs as a spectrum from mild hepatic steatosis only, to non-alcoholic steatohepatitis (NASH) characterized by hepatocellular injury and inflammation, to cirrhosis. A diagnosis of NASH with associated fibrosis heralds a more significant prognosis as it is more likely to progressive to cirrhosis with complications of hepatic failure and hepatocellular carcinoma. Currently, the diagnosis of NASH requires a liver biopsy, however, serum based markers of hepatocyte apoptosis such as cytokeratin-18 fragments offer promise as accurate non-invasive diagnostic tests. Treatment of NAFLD revolves around addressing concomitant metabolic risk factors and improving insulin resistance through weight loss measures and exercise. Insulin sensitizing agents such as pioglitazone and anti-oxidant agents such as vitamin E show some promise in improving liver histology in patients with NASH, however, the long-term benefit of these medications has not been demonstrated.
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Cites
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Cited by
Wang, Q., Ou, Y., Hu, G., Wen, C., Yue, S., Chen, C., Xu, L., Xie, J., Dai, H., Xiao, H., et al. (2020) · British Journal of Pharmacology · doi:10.1111/bph.14938 · Cited by 309
The role of growth hormone and insulin-like growth factor-I in the liver
Takahashi, Y. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18071447 · Cited by 193
IGF-I induces senescence of hepatic stellate cells and limits fibrosis in a p53-dependent manner
Nishizawa, H., Iguchi, G., Fukuoka, H., Takahashi, M., Suda, K., Bando, H., Matsumoto, R., Yoshida, K., Odake, Y., Ogawa, W., et al. (2016) · Scientific Reports · doi:10.1038/srep34605 · Cited by 164
Chen, H., Wang, J., Li, Z., Lam, C. W. K., Xiao, Y., Wu, Q., & Zhang, W. (2019) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph16122192 · Cited by 112
Postprandial lipemia as a cardiometabolic risk factor
Pirillo, A., Norata, G. D., & Catapano, A. L. (2014) · Current Medical Research and Opinion · doi:10.1185/03007995.2014.909394 · Cited by 108
Metadata
- Authors
- Smith, B. W., & Adams, L. A.
- Venue
- Critical Reviews in Clinical Laboratory Sciences
- Publisher
- Informa UK Limited
- Published
- 2011-06
- Volume
- 48
- Issue
- 3
- Pages
- 97-113
- ISSN
- 1040-8363 (ISSN-L)
- 1549-781X
- OpenAlex
- W1986800512
- Cited by
- 285
- References
- 41
- FWCI
- 2.76
- Type
- journal article
- Language
- en
- Open access
- closed
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