VILLANOVA ON THE HUB PARALLELS DOWNLOAD LICENSE

VILLANOVA ON THE HUB PARALLELS DOWNLOAD LICENSE

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Ĭircumstances that determine the severity of NAFLD, including the role of nutrition, gender, and plasma lipid levels, remain to be determined. ©2011 Comhair et al licensee BioMed Central Ltd. (lyso-) phosphatidic acid, lysophosphatidylcholine, diacylglycerols, and ceramides) of enhanced fatty-acid metabolism may be responsible for liver damage (lipo-toxicity hypothesis). Alternatively, harmful side products (e.g. Lipid accumulation alone is benign, but may sensitize the liver to hepatic injury (2-hit hypothesis). The central feature of NAFLD is a disturbed fatty-acid metabolism with hepatic lipid accumulation. The increased prevalence of NAFLD is a concomitant effect of the increased incidence of obesity and a feature ofĭepartment of Anatomy & Embryology, Maastricht University, Maastricht, The Netherlandsįulllist of author information is available at the end of the article Non-alcoholic fatty liver disease (NAFLD) refers to the non-physiological accumulation of fat in the liver.

The fatty-acid saturation of the diet hardly affected hepatic steatosis or inflammation. Conclusions: Dietary cholesterol plays a determining, independent role in inflammation, especially in female mice. Liver inflammation was dependent on genotype (APOE2ki > wild type), gender (female > male), and cholesterol content (high > low) of the diet, but not on dietary fat composition. Irrespective of the composition of the high-fat diet, oleic acid was the main triglyceride component of liver fat in wild-type and APOE2ki mouse livers. This diet caused a 5-fold increase in liver triglyceride and mead-acid content, and an increased expression of lipogenic genes, suggesting a deficiency in poly-unsaturated fatty acids. APOE2ki mice were protected against high-fat diet-induced steatosis and hyperglycemia, except when fed a hoSO diet. All high-fat diets induced macrovesicular setatosis. The high-fat CB, OO, and SO diets induced hyperglycemia and a 2-fold increase in hepatic fat content in male, but not female wildtype mice (in females, hepatic fat content was similar to that in males fed a high-fat diet). Wild-type mice refused the highly saturated fPF diet. Kupffer cells of inflamed livers were swollen. Plasma cholesterol levels in female, but not male APOE2ki mice correlated significantly with inflammation. Results: Addition of cholesterol to a low-fat diet decreased plasma HDL and increased (V)LDL levels in APOE2ki mice. Plasma and liver triglycerides (concentration and composition), liver inflammation (Ccl2, Cd68, Tnf-a mRNA), and infiltration of macrophages (Cd68, Cd11b immunohistochemistry) and neutrophils (Mpo) were quantified.

The fats were, in order of decreasing saturation, fractionated palm fat (fPF ~95%), cocoa butter (CB ~60%), olive oil (OO -15%), sunflower oil (SO -12%), and high-oleic-acid sunflower oil (hoSO -7%). Methods: High-fat diets (42 en% fat), containing 0.2% cholesterol, were fed to male and female wild-type and hyperlipidemic APOE2ki C57BL/6J mice for three weeks. However, the factors that determine the severity of NAFLD, including the role of nutrition, gender, and plasma lipid levels, remain to be determined. Tine M Comhair1,3'st, Sonia C Garcia Caraballo1'3t, Cornelis HC Dejong2,3, Wouter H Lamers1'3'4, S Eleonore Kohler1,3īackground: The central feature of NAFLD is a disturbed fatty-acid metabolism with hepatic lipid accumulation. Dietary cholesterol, female gender and n-3 fatty acid deficiency are more important factors in the development of non-alcoholic fatty liver disease than the saturation index of the fat

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