E
Elizabeth J. Parks
Researcher at University of Missouri
Publications - 93
Citations - 10745
Elizabeth J. Parks is an academic researcher from University of Missouri. The author has contributed to research in topics: Lipogenesis & Fatty acid. The author has an hindex of 39, co-authored 82 publications receiving 9454 citations. Previous affiliations of Elizabeth J. Parks include University of California, Berkeley & University of Texas Southwestern Medical Center.
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Journal ArticleDOI
Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease.
Kerry L. Donnelly,Coleman Smith,Sarah Jane Schwarzenberg,Jose Jessurun,Mark D. Boldt,Elizabeth J. Parks +5 more
TL;DR: In this article, the authors quantified the biological sources of hepatic and plasma lipoprotein TAG in NAFLD patients, using stable isotopes for four days to label and track serum nonesterified fatty acids (NEFAs), dietary fatty acids, and those derived from the de novo lipogenesis (DNL) pathway, present in liver tissue and lipid TAG.
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Inhibition of oxidation of human low-density lipoprotein by phenolic substances in red wine
TL;DR: In in-vitro studies with phenolic substances in red wine and normal human low-density lipoprotein (LDL) the authors found that red wine inhibits the copper-catalysed oxidation of LDL.
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Increased De Novo Lipogenesis Is a Distinct Characteristic of Individuals With Nonalcoholic Fatty Liver Disease
TL;DR: It is confirmed that those with NAFLD have increased synthesis of fatty acids and lipogenesis, and this findings indicate that lipogenesis might be a therapeutic target forNAFLD.
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Carbohydrate-induced hypertriacylglycerolemia: historical perspective and review of biological mechanisms
TL;DR: The phenomenon of carbohydrate-induced hypertriacylglycerolemia is reviewed, the health effects of which are among the most controversial and important issues in public health nutrition today.
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Excessive hepatic mitochondrial TCA cycle and gluconeogenesis in humans with nonalcoholic fatty liver disease.
TL;DR: It is indicated that mitochondrial oxidative metabolism is ~2-fold greater in those with NAFLD, providing a potential link between IHTG content, oxidative stress, and liver damage.