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      Dietary patterns in relation to hepatic fibrosis among patients with nonalcoholic fatty liver disease

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          Abstract

          Background

          Nonalcoholic fatty liver disease (NAFLD) is a multifactorial disorder that can progress to fibrosis. Several dietary patterns have been associated with histological features of NAFLD. However, little is known about the association between dietary patterns and hepatic fibrosis.

          Purpose

          The current study aimed at identifying the relationship between major dietary patterns and hepatic fibrosis among patients with NAFLD.

          Subjects and methods

          This cross-sectional study included 170 eligible subjects with NAFLD. Diet was evaluated using three 3-day dietary records during a 1-month period. Hepatic fibrosis was diagnosed using Fibroscan. Western, Iranian, and healthy dietary patterns were extracted using factor analysis.

          Results

          After adjustment for other risk factors, adherence to a Western dietary pattern was associated with the higher odds of fibrosis (OR: 4.21; 95% CI: 1.63–8.31), whereas adherence to a healthy dietary pattern was associated with the lower odds of fibrosis (OR: 0.26; 95% CI: 0.10–0.49). Among main food groups, high intake of red meat, hydrogenated fats, and soft drinks was associated with the higher risk of fibrosis, whereas tea and coffee consumption had a protective role in hepatic fibrosis independent of other risk factors.

          Conclusion

          The adherence to a healthy dietary pattern characterized by high intake of low-fat dairies, white meat, nuts, vegetables, fruits, and vegetable oils combined with coffee and tea consumption might be helpful in the nutritional strategies against hepatic fibrosis.

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          Most cited references20

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          Nonalcoholic fatty liver disease, hepatic insulin resistance, and type 2 diabetes.

          Nonalcoholic fatty liver disease (NAFLD), hepatic insulin resistance, and type 2 diabetes are all strongly associated and are all reaching epidemic proportions. Whether there is a causal link between NAFLD and hepatic insulin resistance is controversial. This review will discuss recent studies in both humans and animal models of NAFLD that have implicated increases in hepatic diacylglycerol (DAG) content leading to activation of novel protein kinase Cϵ (PKCϵ) resulting in decreased insulin signaling in the pathogenesis of NAFLD-associated hepatic insulin resistance and type 2 diabetes. The DAG-PKCϵ hypothesis can explain the occurrence of hepatic insulin resistance observed in most cases of NAFLD associated with obesity, lipodystrophy, and type 2 diabetes. © 2013 by the American Association for the Study of Liver Diseases.
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            Reproducibility of transient elastography in the evaluation of liver fibrosis in patients with chronic liver disease.

            Transient elastography (TE) is gaining popularity as a non-invasive method for predicting liver fibrosis, but intraobserver and interobserver agreement and factors influencing TE reproducibility have not been adequately assessed. This study investigated these aspects. Tertiary referral liver unit. Over a 4-month period, 200 patients with chronic liver disease (CLD) with varying aetiology consecutively underwent TE and liver biopsy. TE was performed twice by two different operators either concomitantly or within 3 days of the bioptic procedure (METAVIR classification). Intraobserver and interobserver agreement were analysed using the intraclass correlation coefficient (ICC) and correlated with different patient-related and liver disease-related covariates. 800 TE examinations were performed, with an indeterminate result rate of 2.4%. The overall interobserver agreement ICC was 0.98 (95% CI 0.977 to 0.987). Increased body mass index (>25 kg/m(2)), steatosis, and low staging grades (fibrosis (F) stage 7.9 kPa for F>/=2, >10.3 for F>/=3 and >11.9 for F = 4. TE values assessed by the two raters fell within the same cut-off of fibrosis in 88% of the cases for F>/=2, in 92% for F>/=3 and 91% for F = 4. TE is a highly reproducible and user-friendly technique for assessing liver fibrosis in patients with CLD. However, because TE reproducibility is significantly reduced (p<0.05) in patients with steatosis, increased BMI and lower degrees of hepatic fibrosis, caution is warranted in the clinical use of TE as a surrogate for liver biopsy.
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              Free cholesterol accumulation in hepatic stellate cells: mechanism of liver fibrosis aggravation in nonalcoholic steatohepatitis in mice.

              Although nonalcoholic steatohepatitis (NASH) is associated with hypercholesterolemia, the underlying mechanisms of this association have not been clarified. We aimed to elucidate the precise role of cholesterol in the pathophysiology of NASH. C57BL/6 mice were fed a control, high-cholesterol (HC), methionine-choline-deficient (MCD), or MCD+HC diet for 12 weeks or a control, HC, high-fat (HF), or HF+HC diet for 24 weeks. Increased cholesterol intake accelerated liver fibrosis in both the mouse models without affecting the degree of hepatocellular injury or Kupffer cell activation. The major causes of the accelerated liver fibrosis involved free cholesterol (FC) accumulation in hepatic stellate cells (HSCs), which increased Toll-like receptor 4 protein (TLR4) levels through suppression of the endosomal-lysosomal degradation pathway of TLR4, and thereby sensitized the cells to transforming growth factor (TGF)β-induced activation by down-regulating the expression of bone morphogenetic protein and activin membrane-bound inhibitor. Mammalian-cell cholesterol levels are regulated by way of a feedback mechanism mediated by sterol regulatory element-binding protein 2 (SREBP2), maintaining cellular cholesterol homeostasis. Nevertheless, HSCs were sensitive to FC accumulation because the high intracellular expression ratio of SREBP cleavage-activating protein (Scap) to insulin-induced gene (Insig) disrupted the SREBP2-mediated feedback regulation of cholesterol homeostasis in these cells. HSC activation subsequently enhanced the disruption of the feedback system by Insig-1 down-regulation. In addition, the suppression of peroxisome proliferator-activated receptor γ signaling accompanying HSC activation enhanced both SREBP2 and microRNA-33a signaling. Consequently, FC accumulation in HSCs increased and further sensitized these cells to TGFβ-induced activation in a vicious cycle, leading to exaggerated liver fibrosis in NASH. These characteristic mechanisms of FC accumulation in HSCs are potential targets to treat liver fibrosis in liver diseases including NASH. © 2013 by the American Association for the Study of Liver Diseases.
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                Author and article information

                Journal
                Diabetes Metab Syndr Obes
                Diabetes Metab Syndr Obes
                Diabetes, Metabolic Syndrome and Obesity
                Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy
                Dove Medical Press
                1178-7007
                2019
                12 March 2019
                : 12
                : 315-324
                Affiliations
                [1 ]Department of Nutrition, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran, NematyM@ 123456mums.ac.ir
                [2 ]Department of Biological and Environmental Sciences, Faculty of Life and Medical Sciences, University of Hertfordshire, Hatfield, UK
                [3 ]School of Nutrition, Faculté des Sciences de l’agriculture et de l’alimentation, Université Laval, Quebec, QC, Canada
                [4 ]Department of Gastroenterology and Hepatology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
                Author notes
                Correspondence: Mohsen Nematy, Department of Nutrition, Mashhad Medical School, Paradise Daneshgah, Azadi Square, Mashhad, 91779-48564, Iran, Tel +98 3800 2103, Fax +98 3800 2421, Email NematyM@ 123456mums.ac.ir
                Article
                dmso-12-315
                10.2147/DMSO.S198744
                6420105
                30881075
                6b66b8b3-53f1-4e2c-83fa-66d21f69c57b
                © 2019 Soleimani et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Original Research

                Endocrinology & Diabetes
                liver diseases,nafld,fibrosis,factor analysis,diet,dietary pattern
                Endocrinology & Diabetes
                liver diseases, nafld, fibrosis, factor analysis, diet, dietary pattern

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