Increase in long-chain polyunsaturated fatty acid n - 6/n - 3 ratio in relation to hepatic steatosis in patients with non-alcoholic fatty liver disease.
By J. Araya, R. Rodrigo, L. Videla, L. Thielemann, M. Orellana, P. Pettinelli, J. Poniachik. Clinical science, 2004
687 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Nutrition and Dietetics
View Paper: https://www.semanticscholar.org/paper/68601db947ac2c40beb2e673a83d2bf451939fc8
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In Endocrinology, Diabetes and Metabolism
In Epidemiology
Citations in the corpus
- Mouse models in non‐alcoholic fatty liver disease and steatohepatitis research (2006, background): “Accumulation of excess oleic acid (a product of de novo fatty acid synthesis) has been demonstrated in both humans and murine models of steatosis (Shimomura et al. 1998a; Araya et al. 2004).”
- Molecular mediators of hepatic steatosis and liver injury. (2004, neutral): “Humans (16) and mice (17) with hepatic steatosis accumulate excess oleic acid, the end-product of de novo fatty acid synthesis.”
- Nonalcoholic fatty liver disease: pathology and pathogenesis. (2010, background): “In NAFLD patients, a relative depletion of PUFA, particularly longchain PUFA of the n-3 and n-6 class, has been observed (67).”