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https://www.readbyqxmd.com/read/29122391/genetics-and-epigenetics-of-nafld-and-nash-clinical-impact
#1
REVIEW
Mohammed Eslam, Luca Valenti, Stefano Romeo
Non-alcoholic fatty liver disease (NAFLD) is now recognised as the most common liver disease worldwide. It encompasses a broad spectrum of conditions, from simple steatosis, through non-alcoholic steatohepatitis, to fibrosis and ultimately cirrhosis and hepatocellular carcinoma. A hallmark of NAFLD is the substantial inter-patient variation in disease progression. NAFLD is considered a complex disease trait such that interactions between the environment and a susceptible polygenic host background determine disease phenotype and influence progression...
November 2, 2017: Journal of Hepatology
https://www.readbyqxmd.com/read/29083408/exome-wide-association-study-of-plasma-lipids-in-300-000-individuals
#2
Dajiang J Liu, Gina M Peloso, Haojie Yu, Adam S Butterworth, Xiao Wang, Anubha Mahajan, Danish Saleheen, Connor Emdin, Dewan Alam, Alexessander Couto Alves, Philippe Amouyel, Emanuele Di Angelantonio, Dominique Arveiler, Themistocles L Assimes, Paul L Auer, Usman Baber, Christie M Ballantyne, Lia E Bang, Marianne Benn, Joshua C Bis, Michael Boehnke, Eric Boerwinkle, Jette Bork-Jensen, Erwin P Bottinger, Ivan Brandslund, Morris Brown, Fabio Busonero, Mark J Caulfield, John C Chambers, Daniel I Chasman, Y Eugene Chen, Yii-Der Ida Chen, Rajiv Chowdhury, Cramer Christensen, Audrey Y Chu, John M Connell, Francesco Cucca, L Adrienne Cupples, Scott M Damrauer, Gail Davies, Ian J Deary, George Dedoussis, Joshua C Denny, Anna Dominiczak, Marie-Pierre Dubé, Tapani Ebeling, Gudny Eiriksdottir, Tõnu Esko, Aliki-Eleni Farmaki, Mary F Feitosa, Marco Ferrario, Jean Ferrieres, Ian Ford, Myriam Fornage, Paul W Franks, Timothy M Frayling, Ruth Frikke-Schmidt, Lars G Fritsche, Philippe Frossard, Valentin Fuster, Santhi K Ganesh, Wei Gao, Melissa E Garcia, Christian Gieger, Franco Giulianini, Mark O Goodarzi, Harald Grallert, Niels Grarup, Leif Groop, Megan L Grove, Vilmundur Gudnason, Torben Hansen, Tamara B Harris, Caroline Hayward, Joel N Hirschhorn, Oddgeir L Holmen, Jennifer Huffman, Yong Huo, Kristian Hveem, Sehrish Jabeen, Anne U Jackson, Johanna Jakobsdottir, Marjo-Riitta Jarvelin, Gorm B Jensen, Marit E Jørgensen, J Wouter Jukema, Johanne M Justesen, Pia R Kamstrup, Stavroula Kanoni, Fredrik Karpe, Frank Kee, Amit V Khera, Derek Klarin, Heikki A Koistinen, Jaspal S Kooner, Charles Kooperberg, Kari Kuulasmaa, Johanna Kuusisto, Markku Laakso, Timo Lakka, Claudia Langenberg, Anne Langsted, Lenore J Launer, Torsten Lauritzen, David C M Liewald, Li An Lin, Allan Linneberg, Ruth J F Loos, Yingchang Lu, Xiangfeng Lu, Reedik Mägi, Anders Malarstig, Ani Manichaikul, Alisa K Manning, Pekka Mäntyselkä, Eirini Marouli, Nicholas G D Masca, Andrea Maschio, James B Meigs, Olle Melander, Andres Metspalu, Andrew P Morris, Alanna C Morrison, Antonella Mulas, Martina Müller-Nurasyid, Patricia B Munroe, Matt J Neville, Jonas B Nielsen, Sune F Nielsen, Børge G Nordestgaard, Jose M Ordovas, Roxana Mehran, Christoper J O'Donnell, Marju Orho-Melander, Cliona M Molony, Pieter Muntendam, Sandosh Padmanabhan, Colin N A Palmer, Dorota Pasko, Aniruddh P Patel, Oluf Pedersen, Markus Perola, Annette Peters, Charlotta Pisinger, Giorgio Pistis, Ozren Polasek, Neil Poulter, Bruce M Psaty, Daniel J Rader, Asif Rasheed, Rainer Rauramaa, Dermot F Reilly, Alex P Reiner, Frida Renström, Stephen S Rich, Paul M Ridker, John D Rioux, Neil R Robertson, Dan M Roden, Jerome I Rotter, Igor Rudan, Veikko Salomaa, Nilesh J Samani, Serena Sanna, Naveed Sattar, Ellen M Schmidt, Robert A Scott, Peter Sever, Raquel S Sevilla, Christian M Shaffer, Xueling Sim, Suthesh Sivapalaratnam, Kerrin S Small, Albert V Smith, Blair H Smith, Sangeetha Somayajula, Lorraine Southam, Timothy D Spector, Elizabeth K Speliotes, John M Starr, Kathleen E Stirrups, Nathan Stitziel, Konstantin Strauch, Heather M Stringham, Praveen Surendran, Hayato Tada, Alan R Tall, Hua Tang, Jean-Claude Tardif, Kent D Taylor, Stella Trompet, Philip S Tsao, Jaakko Tuomilehto, Anne Tybjaerg-Hansen, Natalie R van Zuydam, Anette Varbo, Tibor V Varga, Jarmo Virtamo, Melanie Waldenberger, Nan Wang, Nick J Wareham, Helen R Warren, Peter E Weeke, Joshua Weinstock, Jennifer Wessel, James G Wilson, Peter W F Wilson, Ming Xu, Hanieh Yaghootkar, Robin Young, Eleftheria Zeggini, He Zhang, Neil S Zheng, Weihua Zhang, Yan Zhang, Wei Zhou, Yanhua Zhou, Magdalena Zoledziewska, Joanna M M Howson, John Danesh, Mark I McCarthy, Chad A Cowan, Goncalo Abecasis, Panos Deloukas, Kiran Musunuru, Cristen J Willer, Sekar Kathiresan
We screened variants on an exome-focused genotyping array in >300,000 participants (replication in >280,000 participants) and identified 444 independent variants in 250 loci significantly associated with total cholesterol (TC), high-density-lipoprotein cholesterol (HDL-C), low-density-lipoprotein cholesterol (LDL-C), and/or triglycerides (TG). At two loci (JAK2 and A1CF), experimental analysis in mice showed lipid changes consistent with the human data. We also found that: (i) beta-thalassemia trait carriers displayed lower TC and were protected from coronary artery disease (CAD); (ii) excluding the CETP locus, there was not a predictable relationship between plasma HDL-C and risk for age-related macular degeneration; (iii) only some mechanisms of lowering LDL-C appeared to increase risk for type 2 diabetes (T2D); and (iv) TG-lowering alleles involved in hepatic production of TG-rich lipoproteins (TM6SF2 and PNPLA3) tracked with higher liver fat, higher risk for T2D, and lower risk for CAD, whereas TG-lowering alleles involved in peripheral lipolysis (LPL and ANGPTL4) had no effect on liver fat but decreased risks for both T2D and CAD...
October 30, 2017: Nature Genetics
https://www.readbyqxmd.com/read/28989566/regional-differences-in-genetic-susceptibility-to-non-alcoholic-liver-disease-in-two-distinct-indian-ethnicities
#3
Govardhan Bale, Avanthi Urmila Steffie, Vishnubhotla Venkata Ravi Kanth, Padaki Nagaraja Rao, Mithun Sharma, Mitnala Sasikala, Duvvur Nageshwar Reddy
AIM: To validate the association of variants in PNPLA3 (rs2281135) and TM6SF2 (rs58542926) genes with ultrasound detected non-alcoholic fatty liver disease (NAFLD). METHODS: A total of 503 individuals with and without fatty infiltration were recruited. Fatty infiltration was confirmed based on ultrasound findings. Anthropometric data and blood samples were collected from the study group. DNA was isolated from peripheral blood, quality and quantity was assessed by gel electrophoresis and spectrophotometer respectively...
September 18, 2017: World Journal of Hepatology
https://www.readbyqxmd.com/read/28972878/role-of-nutrition-gene-polymorphism-and-gut-microbiota-in-non-alcoholic-fatty-liver-disease
#4
Lingbo Kong, Yu Lu, Siyu Zhang, Yuemin Nan, Liang Qiao
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in the world. The nutrients play important roles in the development and progression of NAFLD. High-calorie diet, especially the diet rich in saturated fatty acids and cholesterol, as well as sugary drinks with high fructose content, induces hepatic steatosis and triggers progression of steatohepatitis, fibrosis, and even hepatocellular carcinoma. Disordered micronutrient status and gut microbiota are also involved in the pathogenesis of NAFLD...
September 2017: Discovery Medicine
https://www.readbyqxmd.com/read/28950858/identification-of-deleterious-rare-variants-in-mttp-pnpla3-and-tm6sf2-in-japanese-males-and-association-studies-with-nafld
#5
Supichaya Boonvisut, Ken Yoshida, Kazuhiro Nakayama, Kazuhisa Watanabe, Hiroshi Miyashita, Sadahiko Iwamoto
BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a disorder characterized by excessive fat deposits in hepatocytes without excessive alcohol intake. NAFLD is influenced by genetic factors, and the heritability has been estimated at 0.35 to 0.6 by twin studies. We explored rare variants in known NAFLD-associated genes to investigate whether these rare variants are involved in the susceptibility to NAFLD. METHODS: The target genes for re-sequencing were PNPLA3, TM6SF2, and MTTP...
September 26, 2017: Lipids in Health and Disease
https://www.readbyqxmd.com/read/28839198/the-effect-of-the-tm6sf2-e167k-variant-on-liver-steatosis-and-fibrosis-in-patients-with-chronic-hepatitis-c-a-meta-analysis
#6
Zhengtao Liu, Shuping Que, Lin Zhou, Shusen Zheng, Stefano Romeo, Adil Mardinoglu, Luca Valenti
The impact of Transmembrane 6 superfamily member 2 (TM6SF2) E167K variant, which causes hepatocellular fat retention by altering lipoprotein secretion, on liver damage and metabolic traits in chronic hepatitis C patients is still debated. We performed a systematic review and meta-analysis to clarify this relationship. Four studies with a total of 4325 patients were included. The risk of histologically-determined advanced steatosis, fibrosis, and cirrhosis (but not of severe inflammation) were increased in carriers of the TM6SF2 variant (P < 0...
August 24, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28805745/insulin-resistance-and-nafld-a-dangerous-liaison-beyond-the-genetics
#7
REVIEW
Melania Manco
Over the last decade, the understanding of the association between insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD) has dramatically evolved. There is clear understanding that carriers of some common genetic variants, i.e., the patatin-like phospholipase domain-containing 3 (PNPLA3) or the transmembrane 6 superfamily member 2 (TM6SF2) are at risk of developing severe forms of NAFLD even in the presence of reduced or absent IR. In contrast, there are obese patients with "metabolic" (non-genetically driven) NAFLD who present severe IR...
August 14, 2017: Children
https://www.readbyqxmd.com/read/28711549/a-case-of-hypocholesterolemia-and-steatosis-in-a-carrier-of-a-pcsk9-loss-of-function-mutation-and-polymorphisms-predisposing-to-nonalcoholic-fatty-liver-disease
#8
Mathilde Di Filippo, Benoit Vokaer, Nabil G Seidah
We report a new case of hypobetalipoproteinemia in a 44-year-old man of Peruvian origin exhibiting a heterozygous PCSK9 missense mutation (c.946 G>T, p. Gly316Cys). In vitro functional studies demonstrated that this mutation leads to a loss of function of PCSK9 on low-density lipoprotein receptor degradation. This patient exhibited liver steatosis; he was neither diabetic, nor obese or alcoholic, but is a carrier of 2 polymorphisms, p.Ile148Met (rs738409) and p.Glu167Lys (rs58542926) on PNPLA3 and TM6SF2 gene, respectively, previously shown to be associated with nonalcoholic steatosis and fibrosis evolution...
June 13, 2017: Journal of Clinical Lipidology
https://www.readbyqxmd.com/read/28674415/mboat7-rs641738-variant-and-hepatocellular-carcinoma-in-non-cirrhotic-individuals
#9
Benedetta Donati, Paola Dongiovanni, Stefano Romeo, Marica Meroni, Misti McCain, Luca Miele, Salvatore Petta, Silvia Maier, Chiara Rosso, Laura De Luca, Ester Vanni, Stefania Grimaudo, Renato Romagnoli, Fabio Colli, Flaminia Ferri, Rosellina Margherita Mancina, Paula Iruzubieta, Antonio Craxi, Anna Ludovica Fracanzani, Antonio Grieco, Stefano Ginanni Corradini, Alessio Aghemo, Massimo Colombo, Giorgio Soardo, Elisabetta Bugianesi, Helen Reeves, Quentin M Anstee, Silvia Fargion, Luca Valenti
Nonalcoholic fatty liver disease (NAFLD) represents an emerging cause of hepatocellular carcinoma (HCC), especially in non-cirrhotic individuals. The rs641738 C > T MBOAT7/TMC4 variant predisposes to progressive NAFLD, but the impact on hepatic carcinogenesis is unknown. In Italian NAFLD patients, the rs641738 T allele was associated with NAFLD-HCC (OR 1.65, 1.08-2.55; n = 765), particularly in those without advanced fibrosis (p < 0.001). The risk T allele was linked to 3'-UTR variation in MBOAT7 and to reduced MBOAT7 expression in patients without severe fibrosis...
July 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28645116/the-additive-effects-of-the-tm6sf2-e167k-and-pnpla3-i148m-polymorphisms-on-lipid-metabolism
#10
Lizhen Chen, Shuixian Du, Linlin Lu, Zhonghua Lin, Wenwen Jin, Doudou Hu, Xiangjun Jiang, Yongning Xin, Shiying Xuan
There is a genetic susceptibility for nonalcoholic fatty liver disease (NAFLD). To examine the role of genetic factors in the disease, a Bayesian analysis was performed to model gene relationships in NAFLD pathogenesis. The Bayesian analysis indicated a potential gene interaction between the TM6SF2 and PNPLA3 genes. Next, to explore the underlying mechanism at the cellular level, we evaluated the additive effects between the TM6SF2 E167K and PNPLA3 I148M polymorphisms on lipid metabolism. Hepa 1-6 cells were transfected with a control vector or with overexpression vectors for TM6SF2/PNPLA3-wild type, TM6SF2-mutant type, PNPLA3-mutant type, or TM6SF2/PNPLA3-mutant type...
June 14, 2017: Oncotarget
https://www.readbyqxmd.com/read/28554682/liver-and-cardiovascular-damage-in-patients-with-lean-nonalcoholic-fatty-liver-disease-and-association-with-visceral-obesity
#11
Anna Ludovica Fracanzani, Salvatore Petta, Rosa Lombardi, Giuseppina Pisano, Maurizio Russello, Dario Consonni, Vito Di Marco, Calogero Cammà, Laura Mensi, Paola Dongiovanni, Luca Valenti, Antonio Craxì, Silvia Fargion
BACKGROUND & AIMS: Lean nonalcoholic fatty liver disease (NAFLD) is defined as NAFLD that develops in patients with a body mass index (BMI) less than 25 kg/m(2). We investigated the differences between lean NAFLD and NAFLD in overweight and obese persons, factors associated with the severity of liver and cardiovascular disease, and the effects of visceral obesity. METHODS: We performed a retrospective cohort study of 669 consecutive patients with biopsy-proven NAFLD seen at 3 liver centers in Italy...
May 26, 2017: Clinical Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28539357/novel-association-of-tm6sf2-rs58542926-genotype-with-increased-serum-tyrosine-levels-and-decreased-apob-100-particles-in-finns
#12
Daniel Seung Kim, Anne U Jackson, Yatong K Li, Heather M Stringham, Johanna Kuusisto, Antti J Kangas, Pasi Soininen, Mika Ala-Korpela, Charles F Burant, Veikko Salomaa, Michael Boehnke, Markku Laakso, Elizabeth K Speliotes
A glutamate-to-lysine variant (rs58542926-T) in transmembrane 6 superfamily member 2 (TM6SF2) is associated with increased fatty liver disease and diabetes in conjunction with decreased cardiovascular disease risk. To identify mediators of the effects of TM6SF2, we tested for associations between rs58542926-T and serum lipoprotein/metabolite measures in cross-sectional data from nondiabetic statin-naïve participants. We identified independent associations between rs58542926-T and apoB-100 particles (β = -0...
July 2017: Journal of Lipid Research
https://www.readbyqxmd.com/read/28464257/significant-positive-association-of-endotoxemia-with-histological-severity-in-237-patients-with-non-alcoholic-fatty-liver-disease
#13
J Pang, W Xu, X Zhang, G L-H Wong, A W-H Chan, H-Y Chan, C-H Tse, S S-T Shu, P C-L Choi, H L-Y Chan, J Yu, V W-S Wong
BACKGROUND: Patients with nonalcoholic steatohepatitis (NASH) have gut dysbiosis and intestinal bacterial overgrowth. AIM: To test the hypothesis that endotoxemia is associated with the histological severity of nonalcoholic fatty liver disease (NAFLD) and determine factors associated with endotoxemia. METHODS: The endotoxemia markers lipopolysaccharide-binding protein (LBP) and endotoxin levels were measured in 237 NAFLD patients 1 day before liver biopsy...
July 2017: Alimentary Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/28449094/hepatic-tm6sf2-overexpression-affects-cellular-apob-trafficking-plasma-lipid-levels-hepatic-steatosis-and-atherosclerosis
#14
Nicole Ehrhardt, Michael E Doche, Shuang Chen, Hui Z Mao, Meghan T Walsh, Candy Bedoya, Maha Guindi, Weidong Xiong, Joseph Ignatius Irudayam, Jahangir Iqbal, Sebastien Fuchs, Samuel W French, M Mahmood Hussain, Moshe Arditi, Vaithilingaraja Arumugaswami, Miklós Péterfy
The human transmembrane 6 superfamily member 2 (TM6SF2) gene has been implicated in plasma lipoprotein metabolism, alcoholic and non-alcoholic fatty liver disease and myocardial infarction in multiple genome-wide association studies. To investigate the role of Tm6sf2 in metabolic homeostasis, we generated mice with elevated expression using adeno-associated virus (AAV)-mediated gene delivery. Hepatic overexpression of mouse Tm6sf2 resulted in phenotypes previously observed in Tm6sf2-deficient mice including reduced plasma lipid levels, diminished hepatic triglycerides secretion and increased hepatosteatosis...
July 15, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28436986/adiposity-amplifies-the-genetic-risk-of-fatty-liver-disease-conferred-by-multiple-loci
#15
MULTICENTER STUDY
Stefan Stender, Julia Kozlitina, Børge G Nordestgaard, Anne Tybjærg-Hansen, Helen H Hobbs, Jonathan C Cohen
Complex traits arise from the interplay between genetic and environmental factors. The actions of these factors usually appear to be additive, and few compelling examples of gene-environment synergy have been documented. Here we show that adiposity significantly amplifies the effect of three sequence variants (encoding PNPLA3 p.I148M, TM6SF2 p.E167K, and GCKR p.P446L) associated with nonalcoholic fatty liver disease (NAFLD). Synergy between adiposity and genotype promoted the full spectrum of NAFLD, from steatosis to hepatic inflammation to cirrhosis...
June 2017: Nature Genetics
https://www.readbyqxmd.com/read/28434889/depletion-of-tm6sf2-disturbs-membrane-lipid-composition-and-dynamics-in-huh7-hepatoma-cells
#16
Hanna Ruhanen, P A Nidhina Haridas, Eeva-Liisa Eskelinen, Ove Eriksson, Vesa M Olkkonen, Reijo Käkelä
A polymorphism of TM6SF2 associates with hepatic lipid accumulation and reduction of triacylglycerol (TAG) secretion, but the function of the encoded protein has remained enigmatic. We studied the effect of stable TM6SF2 knock-down on the lipid content and composition, mitochondrial fatty acid oxidation and organelle structure of HuH7 hepatoma cells. Knock-down of TM6SF2 resulted in intracellular accumulation of TAGs, cholesterol esters, phosphatidylcholine (PC) and phosphatidylethanolamine. In all of these lipid classes, polyunsaturated lipid species were significantly reduced while saturated and monounsaturated species increased their proportions...
July 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28407767/e167k-polymorphism-of-tm6sf2-gene-affects-cell-cycle-of-hepatocellular-carcinoma-cell-hepa-1-6
#17
Shuixian Du, Linlin Lu, Yingxia Miao, Wenwen Jin, Changfei Li, Yongning Xin, Shiying Xuan
BACKGROUND: Some studties reported that the polymorphism of TM6SF2 gene E167K affects the occurrence and the progression of hepatocytes carcinoma (hepatocellular, HCC). In oeder to investigate the effects of the polymorphism of TM6SF2 gene E167K in the pathogenesis of HCC, we explored its influence on the cell cycle in hepatocellular carcinoma cell HEPA1-6. METHODS: HEPA 1-6 cells which could respectively overexpress TM6SF2 wild type and E167K variant were cultured and HEPA 1-6 cells with zero load plasmids were used as matched control...
April 13, 2017: Lipids in Health and Disease
https://www.readbyqxmd.com/read/28362682/genetic-determinants-of-circulating-lipoproteins-in-nonalcoholic-fatty-liver-disease
#18
Zhenghui G Jiang, Elliot B Tapper, Misung Kim, Margery A Connelly, Sarah A Krawczyk, Eric U Yee, Mark A Herman, Kenneth J Mukamal, Michelle Lai
BACKGROUND: Recent genome-wide association studies have identified 2 genetic polymorphisms in association with nonalcoholic fatty liver disease (NAFLD): patatin-like phospholipase domain containing 3 (PNPLA3) and transmembrane 6 superfamily member 2 (TM6SF2), both of which appear to influence the production of very low density lipoprotein (VLDL). The impact of these genetic variations on lipoprotein metabolism in the setting of nonalcoholic steatohepatitis and liver fibrosis are not fully characterized...
March 30, 2017: Journal of Clinical Gastroenterology
https://www.readbyqxmd.com/read/28303724/non-alcoholic-fatty-liver-disease-nafld-pathogenesis-classification-and-effect-on-drug-metabolizing-enzymes-and-transporters
#19
Enoch Cobbina, Fatemeh Akhlaghi
Non-alcoholic fatty liver disease (NAFLD) is a spectrum of liver disorders. It is defined by the presence of steatosis in more than 5% of hepatocytes with little or no alcohol consumption. Insulin resistance, the metabolic syndrome or type 2 diabetes and genetic variants of PNPLA3 or TM6SF2 seem to play a role in the pathogenesis of NAFLD. The pathological progression of NAFLD follows tentatively a "three-hit" process namely steatosis, lipotoxicity and inflammation. The presence of steatosis, oxidative stress and inflammatory mediators like TNF-α and IL-6 has been implicated in the alterations of nuclear factors such as CAR, PXR, PPAR-α in NAFLD...
May 2017: Drug Metabolism Reviews
https://www.readbyqxmd.com/read/28242789/tm6sf2-rs58542926-variant-affects-postprandial-lipoprotein-metabolism-and-glucose-homeostasis-in-nafld
#20
Giovanni Musso, Ugo Cipolla, Maurizio Cassader, Silvia Pinach, Francesca Saba, Franco De Michieli, Elena Paschetta, Daria Bongiovanni, Luciana Framarin, Nicola Leone, Mara Berrutti, Floriano Rosina, Stefania Corvisieri, Federica Molinaro, Antonio Sircana, Roberto Gambino
Mechanisms underlying the opposite effects of transmembrane 6 superfamily member 2 (TM6SF2) rs58542926 C>T polymorphism on liver injury and cardiometabolic risk in nonalcoholic fatty liver disease (NAFLD) are unclear. We assessed the impact of this polymorphism on postprandial lipoprotein metabolism, glucose homeostasis, and nutrient oxidation in NAFLD. Sixty nonobese nondiabetic normolipidemic biopsy-proven NAFLD patients and 60 matched controls genotyped for TM6SF2 C>T polymorphism underwent: indirect calorimetry; an oral fat tolerance test with measurement of plasma lipoprotein subfractions, adipokines, and incretin glucose-dependent insulinotropic polypeptide (GIP); and an oral glucose tolerance test with minimal model analysis of glucose homeostasis...
June 2017: Journal of Lipid Research
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