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Non-alcoholic fat liver

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https://www.readbyqxmd.com/read/28928235/testosterone-protects-high-fat-low-carbohydrate-diet-induced-non-alcoholic-fatty-liver-disease-in-castrated-male-rats-mainly-via-modulating-er-stress
#1
Yue Jia, Jennifer Kuang Yee, Christina Wang, Liana Nikolaenko, Maruja Diaz-Arjonilla, Joshua N Cohen, Samuel W French, Peter Y Liu, YanHe Lue, Wai-Nang Paul Lee, Ronald S Swerdloff
We previously showed that testosterone (T) deficiency enhanced high-fat diet (HFD) induced hepatic steatosis in rats that was independent of insulin resistance, and that T replacement reduced hepatic macrovesicular fat accumulation and inflammation. The present report explores the mechanism of T-protective effects on HFD-induced steatohepatitis. Adult male rats were randomized into four treatment groups for 15 weeks (intact rats on regular chow diet or HFD, and castrated rats on HFD with/without T replacement)...
September 19, 2017: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/28925406/abdominal-fat-deposits-determined-by-magnetic-resonance-imaging-in-relation-to-leptin-and-vaspin-levels-as-well-as-insulin-resistance-in-the-general-adult-population
#2
F Genske, J-P Kühn, M Pietzner, G Homuth, W Rathmann, H J Grabe, H Völzke, H Wallaschofski, N Friedrich
BACKGROUND: Various fat depots including visceral (VAT), subcutaneous adipose tissue (SAT) or liver fat content (LFC) were supposed to have different influences on various entities including adipokine levels as well as insulin resistance/sensitivity. Therefore, the aim of the study was to investigate the associations of SAT, VAT and LFC with the levels of leptin and vaspin as well as insulin resistance in a general non-diabetic population. METHODS: In total, 1825 participants of the Study of Health in Pomerania were characterized according to body fat compartments and LFC determined by magnetic resonance imaging...
August 14, 2017: International Journal of Obesity: Journal of the International Association for the Study of Obesity
https://www.readbyqxmd.com/read/28924123/the-improvement-of-the-hepatic-histological-findings-in-a-patient-with-non-alcoholic-steatohepatitis-with-type-2-diabetes-after-the-administration-of-the-sodium-glucose-cotransporter-2-inhibitor-ipragliflozin
#3
Akihiko Takeda, Aya Irahara, Atsuko Nakano, Emi Takata, Yuko Koketsu, Kunie Kimata, Eri Senda, Hajime Yamada, Kazuhito Ichikawa, Takahiro Fujimori, Yoshio Sumida
The patient was a 67-year-old woman with type 2 diabetes and non-alcoholic steatohepatitis (NASH). The administration of the sodium-glucose cotransporter 2 (SGLT2) inhibitor, ipragliflozin improved her liver dysfunction clinically and histologically. The serum alanine aminotransferase (ALT) and ferritin levels decreased to normal limits after treatment for four months. Type IV collagen and hyaluronic acid, both of which were serum fibrotic markers, decreased after treatment. Ultrasonography and computed tomography showed a decrease in the fat deposits in her liver...
September 15, 2017: Internal Medicine
https://www.readbyqxmd.com/read/28923880/impact-of-liver-fat-on-the-differential-partitioning-of-hepatic-triacylglycerol-into-vldl-subclasses-on-high-and-low-sugar-diets
#4
A Margot Umpleby, Fariba Shojaee-Moradie, Barbara Fielding, Xuefei Li, Andrea Marino, Najlaa Alsini, Cheryl Isherwood, Nicola Jackson, Aryati Ahmad, Michael Stolinski, Julie Anne Lovegrove, Sigurd Johnsen, Jeewaka Mendis, John Wright, Malgorzata E Wilinska, Roman Hovorka, Jimmy Bell, Louise E Thomas, Gary Frost, Bruce Arthur Griffin
Dietary sugars are linked to the development of non-alcoholic fatty liver disease (NAFLD) and dyslipidaemia, but it is unknown if NAFLD itself influences the effects of sugars on plasma lipoproteins. To study this further, men with NAFLD (n=11) and low liver fat 'controls' (n= 14) were fed two iso-energetic diets, high or low in sugars (26% or 6% total energy) for 12 weeks, in a randomised, cross-over design. Fasting plasma lipid and lipoprotein kinetics were measured after each diet by stable isotope trace-labelling...
September 18, 2017: Clinical Science (1979-)
https://www.readbyqxmd.com/read/28923496/deficiency-of-the-mitochondrial-nad-kinase-causes-stress-induced-hepatic-steatosis-in-mice
#5
Kezhong Zhang, Hyunbae Kim, Zhiyao Fu, Yining Qiu, Zhao Yang, Jiemei Wang, Deqiang Zhang, Xin Tong, Lei Yin, Jing Li, Jianmei Wu, Nathan R Qi, Sander M Houten, Ren Zhang
BACKGROUND & AIMS: The mitochondrial nicotinamide adenine dinucleotide (NAD) kinase (NADK2, also called MNADK) catalyzes phosphorylation of NAD to yield NADP. Little is known about the functions of mitochondrial NADP and MNADK in liver physiology and pathology. We investigated the effects of reduced mitochondrial NADP by deleting MNADK in mice. METHODS: We generated MNADK-knockout (KO) mice on a C57BL/6NTac background; mice with a wild-type Mnadk gene were used as controls...
September 15, 2017: Gastroenterology
https://www.readbyqxmd.com/read/28919478/atorvastatin-reduces-lipid-accumulation-in-the-liver-by-activating-protein-kinase-a-mediated-phosphorylation-of-perilipin-5
#6
Xing Gao, Yang Nan, Yuanlin Zhao, Yuan Yuan, Bincheng Ren, Chao Sun, Kaiyu Cao, Ming Yu, Xuyang Feng, Jing Ye
Statins have been proven to be effective in treating non-alcoholic fatty liver disease (NAFLD). Recently, it was reported that statins decreased the hepatic expression of perilipin 5 (Plin5), a lipid droplet (LD)-associated protein, which plays critical roles in regulating lipid accumulation and lipolysis in liver. However, the function and regulation mechanism of Plin5 have not yet been well-established in NAFLD treatment with statins. In this study, we observed that atorvastatin moderately reduced the expression of Plin5 in livers without changing the protein level of Plin5 in the hepatic LD fraction of mice fed with high-fat diet (HFD)...
September 12, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28918389/glucagon-like-peptide-1-receptor-agonists-for-the-management-of-obesity-and-non-alcoholic-fatty-liver-disease-a-novel-therapeutic-option
#7
REVIEW
Gauri Dhir, Kenneth Cusi
Obesity is a major risk factor for the development of type 2 diabetes mellitus (T2DM), and is associated with a cluster of metabolic factors that lead to poor cardiovascular outcomes. In non-alcoholic fatty liver disease (NAFLD), liver fat (triglyceride) accumulation closely mirrors adipose tissue dysfunction and insulin resistance in obesity and T2DM. It is now recognized as the most common chronic liver disease in Westernized societies, often progressing to more severe forms of the disease such as nonalcoholic steatohepatitis (NASH), or cirrhosis and hepatocellular carcinoma...
September 15, 2017: Journal of Investigative Medicine: the Official Publication of the American Federation for Clinical Research
https://www.readbyqxmd.com/read/28906444/short-term-intake-of-a-fructose-fat-and-cholesterol-rich-diet-causes-hepatic-steatosis-in-mice-effect-of-antibiotic-treatment
#8
Annette Brandt, Cheng Jun Jin, Katja Nolte, Cathrin Sellmann, Anna Janina Engstler, Ina Bergheim
Intestinal microbiota and barrier functions seem to play an important role in the development of non-alcoholic fatty liver disease (NAFLD). However, whether these changes are an early event in the development of NAFLD or are primarily associated with later stages of the disease, has not yet been clarified. Using a pair-feeding model, we determined the effects of a short-term intake of a fat-, fructose- and cholesterol-rich diet (FFC) on the development of early hepatic steatosis and markers of intestinal barrier function in mice treated with and without non-resorbable antibiotics (AB)...
September 14, 2017: Nutrients
https://www.readbyqxmd.com/read/28900305/berberine-ameliorates-fatty-acid-induced-oxidative-stress-in-human-hepatoma-cells
#9
Yixuan Sun, Xinlu Yuan, Feifei Zhang, Yamei Han, Xinxia Chang, Xi Xu, Yu Li, Xin Gao
Oxidative stress is thought to be critical for the pathogenesis of hepatic steatosis and its progress to non-alcoholic steatohepatitis. Berberine (BBR) can improve hepatic steatosis. In this study, we investigated the role of BBR in ameliorating oxidative stress. Lipid accumulation was measured in the livers of C57BL/6 mice fed a high fat diet (HFD) or a normal diet for 8 weeks, then either received BBR or vehicle for the study duration. Nrf2 distribution was detected in male Sprague-Dawley rats' livers in vivo and in Huh7 cells in vitro...
September 12, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28899784/mir-181b-regulates-steatosis-in-nonalcoholic-fatty-liver-disease-via-targeting-sirt1
#10
Yunxia Wang, Kongxi Zhu, Weihua Yu, Hongjuan Wang, Lan Liu, Qiong Wu, Shuai Li, Jianqiang Guo
Non-alcoholic fatty liver diseases (NAFLD) is one of the leading cause of chronic liver diseases in the world. However, the pathogenesis of NAFLD is still unclear. Emerging studies have demonstrated that microRNAs (miRs) are profoundly involved in NAFLD and related metabolic diseases. Here, we investigated the mechanisms by which miR-181b influences NAFLD via direct targeting SIRT1. The expression of miR181b was up-regulated while SIRT1 was down-regulated in both human NAFLD patients and high fat diet (HFD) induced NAFDL mice model...
September 9, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28895929/effects-of-oral-administration-of-silymarin-in-a-juvenile-murine-model-of-non-alcoholic-steatohepatitis
#11
Veronica Marin, Silvia Gazzin, Sabrina E Gambaro, Matteo Dal Ben, Sonia Calligaris, Monica Anese, Alan Raseni, Claudio Avellini, Pablo J Giraudi, Claudio Tiribelli, Natalia Rosso
The increasing prevalence of non-alcoholic fatty liver disease (NAFLD) in adolescents is challenging the global care system. No therapeutic strategies have been defined so far, and changes in the lifestyle remain the only alternative. In this study, we assessed the protective effects of silymarin in a juvenile non-alcoholic steatohepatitis (NASH) model and the in vitro effects on fat-laden human hepatocytes. C57Bl/6 mice were exposed to HFHC diet immediately after weaning. After eight weeks, animals showed histological signs of NASH...
September 12, 2017: Nutrients
https://www.readbyqxmd.com/read/28895242/hepatocellular-carcinoma-in-a-mouse-model-fed-a-choline-deficient-l-amino-acid-defined-high-fat-diet
#12
Ayae Ikawa-Yoshida, Saori Matsuo, Atsuhiko Kato, Yusuke Ohmori, Atsuko Higashida, Eiji Kaneko, Masahiko Matsumoto
Hepatocellular carcinoma (HCC) is a common cancer worldwide and represents the outcome of the natural history of chronic liver disease. The growing rates of HCC may be partially attributable to increased numbers of people with non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). However, details of the liver-specific molecular mechanisms responsible for the NAFLD-NASH-HCC progression remain unclear, and mouse models that can be used to explore the exact factors that influence the progression of NAFLD/NASH to the more chronic stages of liver disease and subsequent HCC are not yet fully established...
September 12, 2017: International Journal of Experimental Pathology
https://www.readbyqxmd.com/read/28894701/relationship-between-diet-and-non-alcoholic-fatty-liver-disease-a-review-article
#13
REVIEW
Parvin Mirmiran, Zeynab Amirhamidi, Hanieh-Sadat Ejtahed, Zahra Bahadoran, Fereidoun Azizi
BACKGROUND: Diet plays a key role in the development of non-alcoholic fatty liver disease (NAFLD). The aim of this study was to review systematically observational studies available regarding the relationship between food intakes and NAFLD. METHODS: We searched Scopus, PubMed, and Cochrane Library databases to identify English observational studies on food groups, dietary patterns, and NAFLD. Cross-sectional, case-control and cohort studies were selected and then duplication, topic, type of study, study population, variables examined and quality of data reporting of the articles were evaluated...
August 2017: Iranian Journal of Public Health
https://www.readbyqxmd.com/read/28892997/quantification-of-liver-fat-with-mdixon-magnetic-resonance-imaging-comparison-with-the-computed-tomography-and-the-biopsy
#14
Venkatraman Bhat, Sundararaman Velandai, Vikram Belliappa, Jeyeram Illayraja, Karthik Gadabana Halli, Gayathri Gopalakrishnan
INTRODUCTION: Accurate, non-invasive method of fat estimation is a valuable test for evaluation of diseases with abnormal hepatic fat. AIM: To determine the accuracy of mDixon MR technique in assessment of liver fat over CT and to correlate the CT and MRI findings with biopsy. MATERIALS AND METHODS: A prospective observational study was conducted at Imaging Services of Narayana Multispeciality Hospital between March 2011- December 2012. Thirty patients who attended the clinic for non-hepatic complaints were included in the study...
July 2017: Journal of Clinical and Diagnostic Research: JCDR
https://www.readbyqxmd.com/read/28880231/the-impact-of-sex-and-25-oh-d-deficiency-on-metabolic-function-in-mice
#15
Ryan J Giblin, Ellen J Bennett, Graeme R Zosky, Renée M Dwyer
Both dietary fat and vitamin D deficiency have been linked with increased incidence of non-alcoholic fatty liver disease and insulin resistance. While sex differences in disease prevalence and severity are well known, the impact on disease pathogenesis remains unclear. To further explore the effect of these exposures on metabolic function, C57BL/6 male and female mice were weaned onto one of four diets; low fat vitamin D replete, low fat vitamin D deficient, or two high fat diets, one vitamin D replete and one deficient...
September 7, 2017: Nutrients
https://www.readbyqxmd.com/read/28878197/fructose-consumption-lipogenesis-and-non-alcoholic-fatty-liver-disease
#16
REVIEW
Kasper W Ter Horst, Mireille J Serlie
Increased fructose consumption has been suggested to contribute to non-alcoholic fatty liver disease (NAFLD), dyslipidemia, and insulin resistance, but a causal role of fructose in these metabolic diseases remains debated. Mechanistically, hepatic fructose metabolism yields precursors that can be used for gluconeogenesis and de novo lipogenesis (DNL). Fructose-derived precursors also act as nutritional regulators of the transcription factors, including ChREBP and SREBP1c, that regulate the expression of hepatic gluconeogenesis and DNL genes...
September 6, 2017: Nutrients
https://www.readbyqxmd.com/read/28877979/fatty-acids-promote-fatty-liver-disease-via-the-dysregulation-of-3-mercaptopyruvate-sulfurtransferase-hydrogen-sulfide-pathway
#17
Meng Li, Chengfu Xu, Junping Shi, Jiexia Ding, Xingyong Wan, Dahua Chen, Jianguo Gao, Chunxiao Li, Jie Zhang, Yiming Lin, Zhenhua Tu, Xiaoni Kong, Youming Li, Chaohui Yu
OBJECTIVE: Accumulation of free fatty acids (FFAs) in hepatocytes induces lipotoxicity, leading to non-alcoholic fatty liver disease (NAFLD). This study aimed to investigate the underlying mechanisms by which FFA contributes to the pathogenesis of NAFLD via the regulation of 3-mercaptopyruvate sulfurtransferase (MPST), a key enzyme that regulates endogenous hydrogen sulfide (H2S) biosynthesis. DESIGN: Hepatic MPST expression was evaluated in mice and patients with NAFLD...
September 6, 2017: Gut
https://www.readbyqxmd.com/read/28876011/a-study-of-the-prebiotic-like-effects-of-tomato-juice-consumption-in-rats-with-diet-induced-non-alcoholic-fatty-liver-disease-nafld
#18
F J García-Alonso, R González-Barrio, G Martín-Pozuelo, N Hidalgo, I Navarro-González, D Masuero, E Soini, U Vrhovsek, M J Periago
Gut microbiota may play a role in the pathogenesis of NAFLD. We investigated whether tomato juice consumption for 5 weeks could ameliorate high-fat diet-induced alterations in certain intestinal bacterial groups and products arising from their metabolism (short-chain fatty acids and microbial phenolic catabolites). For this, we used a rat model with NAFLD induced by a high-fat diet, involving four experimental groups: NA (standard diet and water), NL (standard diet and tomato juice), HA (high-fat diet and water) and HL (high-fat diet and tomato juice)...
September 6, 2017: Food & Function
https://www.readbyqxmd.com/read/28874443/amelioration-of-diet-induced-steatohepatitis-in-mice-following-combined-therapy-with-aso-fsp27-and-fenofibrate
#19
Ananthi Rajamoorthi, Noemi Arias, Jeannine Basta, Richard G Lee, Ángel Baldán
Non-alcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease. NAFLD progresses from benign steatosis to steatohepatitis (NASH) to cirrhosis, and is linked to hepatocellular carcinoma. No targeted treatment is currently approved for NAFLD/NASH. We showed that fat-specific protein 27 (FSP27), a lipid droplet-associated protein that controls triglyceride turnover in the hepatocyte, is required for fasting- and diet-induced triglyceride accumulation in the liver. However, silencing Fsp27 with antisense oligonucleotides (ASOs) did not improve hepatosteatosis in genetic nor nutritional mouse models of obesity...
September 5, 2017: Journal of Lipid Research
https://www.readbyqxmd.com/read/28859855/degradation-of-phlpp2-by-kctd17-via-a-glucagon-dependent-pathway-promotes-hepatic-steatosis
#20
KyeongJin Kim, Dongryeol Ryu, Paola Dongiovanni, Lale Ozcan, Shruti Nayak, Beatrix Ueberheide, Luca Valenti, Johan Auwerx, Utpal B Pajvani
BACKGROUND & AIMS: Obesity-induced non-alcoholic fatty liver disease (NAFLD) develops, in part, via excess insulin-stimulated hepatic de novo lipogenesis, which increases, paradoxically, in patients with obesity-induced insulin resistance. Pleckstrin homology domain leucine-rich repeat protein phosphatase 2 (PHLPP2) terminates insulin signaling by dephosphorylating Akt; levels of PHLPP2 are reduced in livers from obese mice. We investigated whether loss of hepatic PHLPP2 is sufficient to induce fatty liver in mice, mechanisms of PHLPP2 degradation in fatty liver, and expression of genes that regulate PHLPP2 in livers of patients with NAFLD...
August 28, 2017: Gastroenterology
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