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Modelling of fatty acid metabolism was included in a model of glycolysis by Dash et al. [ 105].
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The rat model of fatty liver was established by feeding a high fat diet.
Finally, a predictive, theoretical model of fatty acid binding was developed that accounted for the observed "overshoot" kinetics.
Glucagon-like peptide-1 (GLP-1) analogues reduce hepatic steatosis, concentrations of liver enzymes, and insulin resistance in murine models of fatty liver disease.
These include molecular level in vitro modeling of fatty acid transfer mechanisms, whole cell studies of fatty acid uptake and intracellular transfer following genetic manipulation of FABP type and amount, and an examination of cells and tissues from animals engineered to lack expression of specific FABPs.
Future improvements in the pure component properties, thermodynamic model and distribution model of fatty acids in the triacylglycerols can increase the use of computational approaches allowing the experiments to be focused on the most promising formulations in terms of melting profile.
Oxidative DNA damage and DNA repair enzyme expression are inversely related in murine models of fatty liver disease.
However, there are important differences in the DNA repair response to oxidant stress among mouse models of fatty liver disease.
To evaluate this hypothesis, we compared mtH2O2 production, MYH expression, oxidative DNA damage, and hepatocyte death in healthy mice and different mouse models of fatty liver disease.
More recently, treatment of mice with IL-6 ameliorated steatosis in different models of fatty liver, including ob/ob mice and ethanol-fed mice [52] [54].
Evidences show that overload of lipids and cholesterol derivatives activate KCs in models of fatty liver disease and steatohepatitis [ 68].
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