Abstract
BackgroundNon-alcoholic and alcoholic fatty liver disease (NAFLD and AFLD, respectively) are major health problems, as patients with either condition can progress to hepatitis, fibrosis, and cirrhosis. Although histologically similar, key differences likely exist in these two models. For example, altered content of several vesicle trafficking proteins have been identified in AFLD, but their content in NAFLD is unknown. In this study, we compared select parameters in NAFLD and AFLD in a rat model.MethodsWe fed either Lieber- DeCarli liquid control or alcohol-containing (35 % as calories) diet (AFLD model) or lean or high-fat (12 or 60 % derived from fat, respectively) pellets (NAFLD model) for 8–10 weeks, n = 8 in each model. Serum, hepatocytes and liver tissue were analyzed. Liver injury markers were measured in serum, triglyceride content and endocytosis (binding and internalization of 125I- asialoorosomucoid) was measured in isolated hepatocytes, and content of selected trafficking proteins (Rab3D, Rab7 and Rab18) were determined in whole liver tissue.ResultsAlthough liver injury markers and triglyceride content were similar in both models, binding and internalization of 125I- asialoorosomucoid was significantly impaired in the hepatocytes from AFLD, but not NAFLD, animals. In addition, protein content of the asialoglycoprotein receptor (ASGPR) and three trafficking proteins, Rab3D, Rab7and Rab18, were significantly decreased after alcohol, but not high-fat feeding. Levels of protein carbonylation, amount of glutathione stores, and lipid peroxidation were similar irrespective of the insult to the livers that resulted in fatty liver.ConclusionImpairments in protein trafficking in AFLD are likely a direct result of alcohol administration, and not a function of fatty liver.
Highlights
Non-alcoholic and alcoholic fatty liver disease (NAFLD and Alcoholic fatty liver disease (AFLD), respectively) are major health problems, as patients with either condition can progress to hepatitis, fibrosis, and cirrhosis
In the present study we asked whether these impairments in asialoglycoprotein receptor (ASGPR) function and RabGTPase content in AFLD would occur in the setting of Non-alcohol fatty liver disease (NAFLD)
Morphology of liver tissue in alcohol and non-alcohol induced fatty liver At the outset of these experimental procedures, we confirmed those rats on the Lieber-DeCarli (EtOH) diet and their cohorts on the high fat diet (HFD) had fatty liver by H&E staining of the liver tissue (Fig. 1)
Summary
Non-alcoholic and alcoholic fatty liver disease (NAFLD and AFLD, respectively) are major health problems, as patients with either condition can progress to hepatitis, fibrosis, and cirrhosis. Fatty liver disease is a prevalent health risk in modern society, can arise from a variety of etiologies, and can progress to hepatitis, fibrosis, and cirrhosis. Fatty liver arising from either alcohol consumption or the over-consumption of a high fat/high sugar diet has a Rasineni et al BMC Gastroenterology (2016) 16:27 similar phenotype in that the hepatocytes accumulate triglycerides. Both are known to result in increased injury markers, such as increased serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP).
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