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      Effects of Omega-3 Fatty Acid in Nonalcoholic Fatty Liver Disease: A Meta-Analysis

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          Abstract

          A meta-analysis was conducted to assess the effect of omega-3 fatty acid supplementation (n-3 PUFAs) in lowering liver fat, liver enzyme (alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyltransferase (GGT) levels), and blood lipids (triglyceride (TG), total cholesterol (TC), high density lipoprotein (HDL), and low density lipoprotein (LDL)) in patients with nonalcoholic fatty liver disease (NAFLD) or nonalcoholic steatohepatitis (NASH). Methods. MEDLINE/PubMed, EMBASE, the Cochrane Central Register of Controlled Trials, CINAHL, Science Citation Index (ISI Web of Science), Chinese Biomedical Literature Database (CBM), and Chinese National Knowledge Infrastructure (CNKI) were searched for relevant randomized controlled trials on the effects of n-3 polyunsaturated fatty acids (PUFAs) in patients with NAFLD from inception to May 2015. Ten studies were included in this meta-analysis. Results. 577 cases of NAFLD/NASH in ten randomized controlled trials (RCTs) were included. The results of the meta-analysis showed that benefit changes in liver fat favored PUFA treatment, and it was also beneficial for GGT, but it was not significant on ALT, AST, TC, and LDL. Conclusions. In this meta-analysis, omega-3 PUFAs improved liver fat, GGT, TG, and HDL in patients with NAFLD/NASH. Therefore, n-3 PUFAs may be a new treatment option for NAFLD.

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          Increase in long-chain polyunsaturated fatty acid n - 6/n - 3 ratio in relation to hepatic steatosis in patients with non-alcoholic fatty liver disease.

          Hepatic steatosis is a major feature associated with NAFLD (non-alcoholic fatty liver disease). The aims of the present study were to assess the levels of PUFA (polyunsaturated fatty acids) in liver total lipids, triacylglycerols (triglycerides) and phospholipids of NAFLD patients in relation to those in adipose tissue and hepatic indexes related to oxidative stress as factors contributing to hepatic steatosis. Eleven control subjects and 19 patients with NAFLD were studied. Analysis of liver and abdominal adipose tissue fatty acids was carried out by GLC. The liver content of protein carbonyl groups and malondialdehyde were taken as indexes related to oxidative stress. NAFLD patients had a depletion in LCPUFA (long-chain PUFA) of the n -6 and n -3 series in liver triacylglycerols, with decreased 20:4, n -6/18:2, n -6 and (20:5, n -3+22:6, n -3)/18:3, n -3 ratios, whereas liver phospholipids contained higher n -6 and lower n -3 LCPUFA. These findings were accompanied by an enhancement of (i) n -6/ n -3 ratio in liver and adipose tissue, (ii) 18:1, n -9 trans levels in adipose tissue, and (iii) hepatic lipid peroxidation and protein oxidation indexes. It is concluded that a marked enhancement in LCPUFA n -6/ n -3 ratio occurs in the liver of NAFLD patients, a condition that may favour lipid synthesis over oxidation and secretion, thereby leading to steatosis. Depletion of hepatic LCPUFA may result from both defective desaturation of PUFA, due to inadequate intake of precursors, such as 18:3, n -3, and higher intake of the 18:1, n -9 trans isomer leading to desaturase inhibition, and from an increased peroxidation of LCPUFA due to oxidative stress.
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            Clinical Review: Nonalcoholic fatty liver disease: a novel cardiometabolic risk factor for type 2 diabetes and its complications.

            Nonalcoholic fatty liver disease (NAFLD) is increasingly diagnosed worldwide and is the most common chronic liver disease in Western countries. In this review, we discuss the role of NAFLD as a novel cardiometabolic risk factor for the development of type 2 diabetes (T2DM) and for the development of major chronic complications and poor glycemic control in people with established T2DM. This is a clinical, narrative review and not a systematic review and meta-analysis. PubMed was extensively searched for articles using the keywords "nonalcoholic fatty liver disease" or "fatty liver" combined with "diabetes risk," "cardiovascular risk," "cardiovascular mortality," "chronic kidney disease," or "diabetic nephropathy" between 1990 and 2012. Articles published in languages other than English were excluded from the analysis. NAFLD exacerbates hepatic insulin resistance and increases the risk of developing T2DM. Growing evidence also indicates that NAFLD may worsen glycemic control in people with T2DM and may contribute to the development and progression of the most important chronic complications of diabetes, such as cardiovascular disease and chronic kidney disease. The adverse impact of NAFLD on risk for T2DM and its major chronic vascular complications deserves particular attention among endocrinologists/cardiologists/hepatologists, in view of the implications for screening and surveillance strategies in the growing number of patients with NAFLD. Clinicians who manage patients with NAFLD should not only focus on liver disease, but should also recognize the increased risk of developing T2DM and its chronic vascular complications and undertake early, aggressive risk factor modification.
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              Dietary habits and nutrient intake in non-alcoholic steatohepatitis.

              Non-alcoholic steatohepatitis (NASH) is one of the most important emerging health issues. Insulin resistance and metabolic syndrome play a central role in the pathogenesis of NASH. Intake of nutrients strongly affects insulin resistance, carbohydrate and lipid metabolism, and hepatic steatosis. However, there are few reports about the intake of various nutrients in non-alcoholic fatty liver disease. In this work, we identified the characteristics of dietary habits and nutrient intake in patients with NASH. Twenty-eight patients with NASH and 18 with simple steatosis (FL) were diagnosed from histologic findings, and their dietary habits and intake of nutrients were analyzed by detailed questioning by physicians and dieticians. There was an excess intake of carbohydrates/energy in patients with NASH 20-59 y of age compared with patients with FL. Among carbohydrates, intake of simple carbohydrates was higher in those with NASH. There also was a low intake of protein/energy in patients with NASH 40-59 y of age and a low intake of zinc in those 20-59 y of age compared with patients with FL. Ratio of intake of polyunsaturated fatty acid to saturated fatty acid was lower in patients with NASH and those with FL compared with the general Japanese subjects. These results suggest that imbalanced diets play important roles in development and progression of NASH and correction of these diets may be necessary in patients with NASH.
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                Author and article information

                Journal
                Gastroenterol Res Pract
                Gastroenterol Res Pract
                GRP
                Gastroenterology Research and Practice
                Hindawi Publishing Corporation
                1687-6121
                1687-630X
                2016
                29 August 2016
                : 2016
                : 1459790
                Affiliations
                1Department of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200072, China
                2The First Clinical Medical College, Nanjing Medical University, Nanjing 210029, China
                3The First Affiliated Hospital of Soochow University, Suzhou 215006, China
                Author notes

                Academic Editor: Michel Kahaleh

                Author information
                http://orcid.org/0000-0002-2954-0559
                http://orcid.org/0000-0003-4429-9043
                http://orcid.org/0000-0002-5658-600X
                Article
                10.1155/2016/1459790
                5019889
                27651787
                47a5c054-6178-49b2-9aec-af0d837cfc3a
                Copyright © 2016 Wenxia Lu et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 21 January 2016
                : 18 July 2016
                Categories
                Research Article

                Gastroenterology & Hepatology
                Gastroenterology & Hepatology

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