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https://www.readbyqxmd.com/read/29404510/interaction-between-the-patatin-like-phospholipase-domain-containing-protein-3-genotype-and-coffee-drinking-and-the-risk-for-acute-alcoholic-hepatitis
#1
Suthat Liangpunsakul, James J Beaudoin, Vijay H Shah, Puneet Puri, Arun J Sanyal, Patrick S Kamath, Spencer G Lourens, Qing Tang, Barry P Katz, David W Crabb, Naga P Chalasani
Only a subset of subjects with excessive alcohol consumption develops alcoholic liver disease (ALD). One of the major risk factors for ALD is the genetic variant of the patatin-like phospholipase domain-containing protein 3 (PNPLA3) gene. Coffee is one of the most commonly consumed beverages, and coffee consumption has been associated with lower levels of serum alanine aminotransferase. The aim of this study was to investigate the role of coffee drinking and PNPLA3 rs738409 and their association with alcoholic hepatitis (AH) in a well-characterized cohort of subjects from the Translational Research and Evolving Alcoholic Hepatitis Treatment consortium...
January 2018: Hepatology Communications
https://www.readbyqxmd.com/read/29397014/host-genetic-factors-associated-with-hepatocellular-carcinoma-in-patients-with-hepatitis-c-virus-infection-a-systematic-review
#2
Alex J Walker, Christian J Peacock, Vincent Pedergnana, William L Irving
Hepatitis C virus (HCV)-infected patients are at risk of developing hepatocellular carcinoma (HCC). Individuals at heightened riskcould be targeted by intensive follow-up surveillance. We have conducted a systematic review of the literature to identify host genetic predisposition to HCC in HCV-infected patients. A comprehensive search of Medline and Embase databases was performed and the strength of evidence of associations for each gene on development of HCC was evaluated. We identified 166 relevant studies, relating to 137 different genes, or combinations thereof...
February 3, 2018: Journal of Viral Hepatitis
https://www.readbyqxmd.com/read/29396131/donor-pnpla3-rs738409-genotype-is-a-risk-factor-for-graft-steatosis-a-post-transplant-biopsy-based-study
#3
Pavel Trunečka, Irena Míková, Dana Dlouhá, Jaroslav A Hubáček, Eva Honsová, Libor Kolesár, Věra Lánská, Soňa Fraňková, Jan Šperl, Milan Jirsa, Rudolf Poledne
BACKGROUND & AIMS: The rs738409 c.444C > G (p.I148M) polymorphism in PNPLA3 is a major factor predisposing to non-alcoholic fatty liver disease. The aim of the study was to clarify the impact of liver and extrahepatic expression of the PNPLA3 p.148M variant on liver graft steatosis after liver transplantation. METHODS: Fat content was assessed in liver biopsies from 176 transplant recipients. During a period of 4 ± 1 years after transplantation, 17 patients developed grade 3 steatosis, 14 patients grade 2 steatosis, 56 patients grade 1 steatosis, and 89 patients grade 0 steatosis...
January 9, 2018: Digestive and Liver Disease
https://www.readbyqxmd.com/read/29385134/risk-estimation-model-for-nonalcoholic-fatty-liver-disease-in-the-japanese-using-multiple-genetic-markers
#4
Takahisa Kawaguchi, Toshihide Shima, Masayuki Mizuno, Yasuhide Mitsumoto, Atsushi Umemura, Yoshihiro Kanbara, Saiyu Tanaka, Yoshio Sumida, Kohichiro Yasui, Meiko Takahashi, Keitaro Matsuo, Yoshito Itoh, Katsutoshi Tokushige, Etsuko Hashimoto, Kendo Kiyosawa, Masanori Kawaguchi, Hiroyuki Itoh, Hirofumi Uto, Yasuji Komorizono, Ken Shirabe, Shiro Takami, Toshinari Takamura, Miwa Kawanaka, Ryo Yamada, Fumihiko Matsuda, Takeshi Okanoue
The genetic factors affecting the natural history of nonalcoholic fatty liver disease (NAFLD), including the development of nonalcoholic steatohepatitis (NASH) and NASH-derived hepatocellular carcinoma (NASH-HCC), are still unknown. In the current study, we sought to identify genetic factors related to the development of NAFLD, NASH, and NASH-HCC, and to establish risk-estimation models for them. For these purposes, 936 histologically proven NAFLD patients were recruited, and genome-wide association (GWA) studies were conducted for 902, including 476 NASH and 58 NASH-HCC patients, against 7,672 general-population controls...
2018: PloS One
https://www.readbyqxmd.com/read/29314568/genetic-determinants-of-hepatic-steatosis-and-serum-cytokeratin-18-fragment-levels-in-taiwanese-children
#5
Yu-Cheng Lin, Pi-Feng Chang, Mei-Hwei Chang, Yen-Hsuan Ni
BACKGROUND/AIMS: There are substantial genetic components contributing to the susceptibility of nonalcoholic NAFLD disease (NAFLD). It has recently been reported that the rs641738 C>T variant in the membrane-bound O-acyltransferase domain-containing protein 7 (MBOAT7) gene increased severity of NAFLD in adults of European descent. We aimed to test the hypothesis that MBOAT7 rs641738 variant would increase hepatic steatosis and hepatocellular injury in obese children. METHODS: A total of 831 obese children aged 7-15 years were recruited...
January 4, 2018: Liver International: Official Journal of the International Association for the Study of the Liver
https://www.readbyqxmd.com/read/29286303/disturbed-vitamin-a-metabolism-in-non-alcoholic-fatty-liver-disease-nafld
#6
REVIEW
Ali Saeed, Robin P F Dullaart, Tim C M A Schreuder, Hans Blokzijl, Klaas Nico Faber
Vitamin A is required for important physiological processes, including embryogenesis, vision, cell proliferation and differentiation, immune regulation, and glucose and lipid metabolism. Many of vitamin A's functions are executed through retinoic acids that activate transcriptional networks controlled by retinoic acid receptors (RARs) and retinoid X receptors (RXRs).The liver plays a central role in vitamin A metabolism: (1) it produces bile supporting efficient intestinal absorption of fat-soluble nutrients like vitamin A; (2) it produces retinol binding protein 4 (RBP4) that distributes vitamin A, as retinol, to peripheral tissues; and (3) it harbors the largest body supply of vitamin A, mostly as retinyl esters, in hepatic stellate cells (HSCs)...
December 29, 2017: Nutrients
https://www.readbyqxmd.com/read/29280273/causal-relationship-of-hepatic-fat-with-liver-damage-and-insulin-resistance-in-nonalcoholic-fatty-liver
#7
P Dongiovanni, S Stender, A Pietrelli, R M Mancina, A Cespiati, S Petta, S Pelusi, P Pingitore, S Badiali, M Maggioni, V Mannisto, S Grimaudo, R M Pipitone, J Pihlajamaki, A Craxi, M Taube, L M S Carlsson, S Fargion, S Romeo, J Kozlitina, L Valenti
BACKGROUND AND AIMS: Nonalcoholic fatty liver disease is epidemiologically associated with hepatic and metabolic disorders. The aim of this study was to examine whether hepatic fat accumulation has a causal role in determining liver damage and insulin resistance. METHODS: We performed a Mendelian randomization analysis using risk alleles in PNPLA3, TM6SF2, GCKR and MBOAT7, and a polygenic risk score for hepatic fat, as instruments. We evaluated complementary cohorts of at-risk individuals and individuals from the general population: 1515 from the liver biopsy cohort (LBC), 3329 from the Swedish Obese Subjects Study (SOS) and 4570 from the population-based Dallas Heart Study (DHS)...
December 27, 2017: Journal of Internal Medicine
https://www.readbyqxmd.com/read/29273888/identification-of-pleiotropic-genetic-variants-affecting-osteoporosis-risk-in-a-korean-elderly-cohort
#8
Eun Pyo Hong, Ka Hyun Rhee, Dong Hyun Kim, Ji Wan Park
Pleiotropy has important implications for understanding the genetic basis and risk assessment of osteoporosis. Our aim was to identify pleiotropic genetic variants associated with the development of osteoporosis and predict osteoporosis risk by leveraging pleiotropic variants. We evaluated the effects of 21 conventional risk factors and 185 single-nucleotide polymorphisms (SNPs) in 63 inflammation- and metabolism-related genes on osteoporosis risk in a community-based Korean cohort study of 1025 participants, the Hallym Aging Study...
December 22, 2017: Journal of Bone and Mineral Metabolism
https://www.readbyqxmd.com/read/29258449/the-rs738409-polymorphism-of-the-pnpla3-gene-is-associated-with-hepatic-steatosis-and-fibrosis-in-brazilian-patients-with-chronic-hepatitis-c
#9
Caroline Manchiero, Arielle Karen da Silva Nunes, Mariana Carvalheiro Magri, Bianca Peixoto Dantas, Celso Carmo Mazza, Antonio Alci Barone, Fátima Mitiko Tengan
BACKGROUND: Prospective studies have shown that 80% of acute hepatitis C virus (HCV) cases progress to chronic infection; approximately 10-20% of patients with these conditions will develop liver cirrhosis within 2 to 3 decades, and 1-5% will develop liver cancer. Some studies have indicated that the rs738409 polymorphism of the PNPLA3 gene is associated with steatosis and the progression of advanced fibrosis. This study assessed the contribution of the PNPLA3 rs738409 polymorphism with regard to the steatosis and degree of liver fibrosis in Brazilian patients diagnosed with chronic hepatitis C...
December 19, 2017: BMC Infectious Diseases
https://www.readbyqxmd.com/read/29228164/liver-fat-content-non-alcoholic-fatty-liver-disease-and-ischaemic-heart-disease-mendelian-randomization-and-meta-analysis-of-279%C3%A2-013-individuals
#10
Bo Kobberø Lauridsen, Stefan Stender, Thomas Skårup Kristensen, Klaus Fuglsang Kofoed, Lars Køber, Børge G Nordestgaard, Anne Tybjærg-Hansen
Aims: In observational studies, non-alcoholic fatty liver disease (NAFLD) is associated with high risk of ischaemic heart disease (IHD). We tested the hypothesis that a high liver fat content or a diagnosis of NAFLD is a causal risk factor for IHD. Methods and results: In a cohort study of the Danish general population (n = 94 708/IHD = 10 897), we first tested whether a high liver fat content or a diagnosis of NAFLD was associated observationally with IHD...
December 8, 2017: European Heart Journal
https://www.readbyqxmd.com/read/29218813/association-of-pnpla3-rs738409-polymorphism-with-liver-steatosis-but-not-with-cirrhosis-in-patients-with-hbv-infection-systematic-review-with-meta-analysis
#11
REVIEW
Saman Ghalamkari, Heidar Sharafi, Seyed Moayed Alavian
BACKGROUND AND AIM: Hepatitis B virus (HBV) infection is a worldwide health issue and is well known to be the main cause of developing secondary liver complications such as cirrhosis and hepatocellular carcinoma (HCC). The PNPLA3 rs738409 polymorphism has been investigated conclusively with occurrence risk of steatosis and cirrhosis. Therefore, performing a meta-analysis of the available studies with the aim of clarifying the association between rs738409 and occurrence risk of steatosis and cirrhosis among HBV-infected patients would be helpful...
December 7, 2017: Journal of Gene Medicine
https://www.readbyqxmd.com/read/29193269/additive-effects-of-pnpla3-and-tm6sf2-on-the-histological-severity-of-non-alcoholic-fatty-liver-disease
#12
Bo Kyung Koo, Sae Kyung Joo, Donghee Kim, Jeong Mo Bae, Jeong Hwan Park, Jung Ho Kim, Won Kim
BACKGROUND AND AIM: We investigated the effects of PNPLA3 rs738409, TM6SF2 rs58542926, and MBOAT7-TMC4 rs641738 variants on metabolic phenotypes and their combined effects on the histological severity of non-alcoholic fatty liver disease (NAFLD). METHODS: We genotyped rs738409, rs58542926, and rs641738 in biopsy-proven NAFLD patients (n = 416) and healthy controls (n = 109). Homeostasis model assessment of insulin resistance (HOMA-IR) and adipose tissue insulin resistance (adipo-IR) were calculated...
November 29, 2017: Journal of Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/29160303/the-pnpla3-i148m-variant-is-associated-with-transaminase-elevations-in-type-2-diabetes-patients-treated-with-basal-insulin-peglispro
#13
S Pillai, S Duvvuru, P Bhatnagar, W Foster, M Farmen, S Shankar, C Harris, E Bastyr, B Hoogwerf, A Haupt
Basal insulin peglispro (BIL) is a novel insulin with hepato-preferential action. In phase 3 trials, BIL showed significantly improved glycemic control but higher levels of transaminases (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)), triglycerides (TGs) and liver fat content (LFC) compared with insulin glargine (GL). As variants in PNPLA3 (I148M) and TM6SF2 (E167K) are associated with nonalcoholic fatty liver disease, we assessed these variants in type 2 diabetes (T2D) patients randomized to receive BIL (n=1822) or GL (n=1270) in three phase 3 trials...
November 21, 2017: Pharmacogenomics Journal
https://www.readbyqxmd.com/read/29158695/pnpla3-expression-and-its-impact-on-the-liver-current-perspectives
#14
REVIEW
Francesca Virginia Bruschi, Matteo Tardelli, Thierry Claudel, Michael Trauner
A single-nucleotide polymorphism occurring in the sequence of the human patatin-like phospholipase domain-containing 3 gene (PNPLA3), known as I148M variant, is one of the best characterized and deeply investigated variants in several clinical scenarios, because of its tight correlation with increased risk for developing hepatic steatosis and more aggressive part of the disease spectrum, such as nonalcoholic steatohepatitis, advanced fibrosis and cirrhosis. Further, the I148M variant is positively associated with alcoholic liver diseases, chronic hepatitis C-related cirrhosis and hepatocellular carcinoma...
2017: Hepatic Medicine: Evidence and Research
https://www.readbyqxmd.com/read/29150621/pnpla3-variant-and-portal-periportal-histological-pattern-in-patients-with-biopsy-proven-non-alcoholic-fatty-liver-disease-a-possible-role-for-oxidative-stress
#15
Guido Carpino, Daniele Pastori, Francesco Baratta, Diletta Overi, Giancarlo Labbadia, Licia Polimeni, Alessia Di Costanzo, Gaetano Pannitteri, Roberto Carnevale, Maria Del Ben, Marcello Arca, Francesco Violi, Francesco Angelico, Eugenio Gaudio
Pathogenesis of non-alcoholic fatty liver disease (NAFLD) is influenced by predisposing genetic variations, dysmetabolism, systemic oxidative stress, and local cellular and molecular cross-talks. Patatin-like phospholipase domain containing 3 (PNPLA3) gene I148M variant is a known determinant of NAFLD. Aims were to evaluate whether PNPLA3 I148M variant was associated with a specific histological pattern, hepatic stem/progenitor cell (HpSC) niche activation and serum oxidative stress markers. Liver biopsies were obtained from 54 NAFLD patients...
November 17, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29128053/nonalcoholic-fatty-liver-disease-and-metabolic-syndrome
#16
REVIEW
Donghee Kim, Alexis Touros, W Ray Kim
Nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome (MS) are highly prevalent, affecting approximately one-third of the US population. The relationship between NAFLD and MS is complex and may be bidirectionally associated. NAFLD is strongly associated with MS, the components of which include abdominal obesity, hyperglycemia, hypertension, and dyslipidemia. NAFLD associated with certain genetic factors such as the PNPLA3 G allele variant is not accompanied by insulin resistance and MS. Lifestyle modification, including diet and physical activity targeting visceral adiposity, remains the standard of care for patients with NAFLD and MS...
February 2018: Clinics in Liver Disease
https://www.readbyqxmd.com/read/29122391/genetics-and-epigenetics-of-nafld-and-nash-clinical-impact
#17
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/29116096/aqp3-is-regulated-by-ppar%C3%AE-and-jnk-in-hepatic-stellate-cells-carrying-pnpla3-i148m
#18
Matteo Tardelli, Francesca V Bruschi, Thierry Claudel, Veronica Moreno-Viedma, Emina Halilbasic, Fabio Marra, Merima Herac, Thomas M Stulnig, Michael Trauner
Aquaglyceroporins (AQPs) allow the movement of glycerol that is required for triglyceride formation in hepatic stellate cells (HSC), as key cellular source of fibrogenesis in the liver. The genetic polymorphism I148M of the patatin-like phospholipase domain-containing 3 (PNPLA3) is associated with hepatic steatosis and its progression to steatohepatitis (NASH), fibrosis and cancer. We aimed to explore the role of AQP3 for HSC activation and unveil its potential interactions with PNPLA3. HSC were isolated from human liver, experiments were performed in primary HSC and human HSC line LX2...
November 7, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29089161/association-between-pnpla3-rs738409-c-g-variant-and-hepatocellular-carcinoma-in-asian-chronic-hepatitis-c-patients-a-longitudinal-study
#19
Yi-Hao Yen, Ming-Chao Tsai, Cheng-Kun Wu, Kuo-Chin Chang, Chao-Hung Hung, King-Wah Chiu, Sheng-Nan Lu, Jing-Houng Wang, Chien-Hung Chen, Kwong-Ming Kee, Yuan-Hung Kuo, Po-Lin Tseng, Ming-Tsung Lin, Chao-Min Huang, Jung-Ting Lin, Tsung-Hui Hu
BACKGROUND/PURPOSE: Prdevious meta-analyses assess whether or not patatin-like phospholipase domain containing 3 (PNPLA3) (rs738409 C > G) was associated with increased risk of hepatocellular carcinoma (HCC) in Caucasians patients with hepatitis C virus (HCV)-related cirrhosis, these meta-analyses did not provide firm conclusions. Only one cross-sectional study involving Asian patients has previously been conducted to explore this issue. We aim to investigate this in a longitudinal cohort of Asian chronic hepatitis C (CHC) patients...
October 28, 2017: Journal of the Formosan Medical Association, Taiwan Yi Zhi
https://www.readbyqxmd.com/read/29083408/exome-wide-association-study-of-plasma-lipids-in-300-000-individuals
#20
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
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