Abstract
BackgroundNonalcoholic fatty liver disease (NAFLD) is one of the most frequent causes of abnormal liver function. Because fatty acids can damage biological membranes, fatty acid accumulation in the liver may be partially responsible for the functional and morphological changes that are observed in nonalcoholic liver disease. The aim of this study was to use gas chromatography-mass spectrometry to evaluate the fatty acid composition of an experimental mouse model of NAFLD induced by high-fat feed and CCl4 and to assess the association between liver fatty acid accumulation and NAFLD. C57BL/6J mice were given high-fat feed for six consecutive weeks to develop experimental NAFLD. Meanwhile, these mice were given subcutaneous injections of a 40% CCl4-vegetable oil mixture twice per week.ResultsA pathological examination found that NAFLD had developed in the C57BL/6J mice. High-fat feed and CCl4 led to significant increases in C14:0, C16:0, C18:0 and C20:3 (P < 0.01), and decreases in C15:0, C18:1, C18:2 and C18:3 (P < 0.01) in the mouse liver. The treatment also led to an increase in SFA and decreases in other fatty acids (UFA, PUFA and MUFA). An increase in the ratio of product/precursor n-6 (C20:4/C18:2) and n-3 ([C20:5+C22:6]/C18:3) and a decrease in the ratio of n-6/n-3 (C20:4/[C20:5+C22:6]) were also observed.ConclusionThese data are consistent with the hypothesis that fatty acids are deranged in mice with non-alcoholic fatty liver injury induced by high-fat feed and CCl4, which may be involved in its pathogenesis and/or progression via an unclear mechanism.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is one of the most frequent causes of abnormal liver function
Histological profile All of the sections in the experimental group exhibited diffuse hepatic steatosis (Figure 1) under a light microscope, whereas no fatty liver was observed in the control group The relative sizes of the hepatic cell nuclei were uneven
In contrast to the control mice, a histological analysis of the livers from the mice treated with a high-fat feed and a hepatotoxin (CCl4) confirmed marked fat accumulation and revealed extensive inflammatory cell infiltration, indicating that diffuse hepatic steatosis with moderate inflammation (NAFLD) had developed
Summary
Nonalcoholic fatty liver disease (NAFLD) is one of the most frequent causes of abnormal liver function. Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of conditions that are histologically characterized by hepatic steatosis in individuals without significant alcohol consumption and with no viral, congenital, or autoimmune liver disease markers [1]. It is associated with insulin resistance and metabolic syndrome [2,3]. The aim of this study was to compare the liver fatty acid profiles and detailed compositions of healthy mice vs mice with an experimental model of NAFLD induced by high-fat feed and CCl4
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