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Glucagon-like peptide-1 (GLP-1) analogues reduce hepatic steatosis, concentrations of liver enzymes, and insulin resistance in murine 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].
In addition, studies on pancreatic carcinogenesis using animal models of fatty pancreas would be helpful to elucidate underlying mechanisms.
Evidences show that overload of lipids and cholesterol derivatives activate KCs in models of fatty liver disease and steatohepatitis [ 68].
Similarly, models of fatty liver disease, e.g. induced by dietary fructose or by lack of leptin showed that occludin protein expression is decreased and portal endotoxin levels are elevated in the small intestine [ 7, 38].
Similar(55)
Finally, a predictive, theoretical model of fatty acid binding was developed that accounted for the observed "overshoot" kinetics.
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.
Modelling of fatty acid metabolism was included in a model of glycolysis by Dash et al. [ 105].
This feature is evaluated both manually by investigating specific pairs of high-scoring metabolites, and then systematically on a literature-curated model of fatty acid synthesis and degradation.
The objective of this study was to determine whether dietary palmitate exerts the same toxicity as carbohydrate-derived palmitate in the MCD model of fatty liver disease.
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