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  1. AU="Umarova, Regina"
  2. AU="Sartre, Milena"
  3. AU="Laemmerer, Anna"
  4. AU="Guedes, Tássia T A M"
  5. AU=Savoie L L
  6. AU="Huang, Tsai-Wei"
  7. AU="Michael Pugliese"
  8. AU="Amador-Sánchez, Yoarhy A"
  9. AU="Lanbo Shi"
  10. AU="Gregg, R J"
  11. AU="Zou, Peiyuan"
  12. AU="Sasha Stevenson"
  13. AU="Boncompagni, Alessandra"
  14. AU="Lewis, Annisa L"
  15. AU="Daniel Freilich"
  16. AU="Glascock, Abigail L"
  17. AU="Gordon Bernard"
  18. AU="Lv, Mengwen"
  19. AU="Rottman Pietrzak, Kathleen A"
  20. AU=Panczak Radoslaw
  21. AU="Hosseini, Seyed Mohammad Hadi"
  22. AU="Noda, Haruna"
  23. AU="Raoul, Cédric"
  24. AU=Wissing Silke AU=Wissing Silke
  25. AU="Chun-Lin Yang"
  26. AU="Romine, Kyle A"
  27. AU="Cunsolo, Vincenzo"
  28. AU="Ba, Aboubacar"
  29. AU="Prisca, Mirandolina"
  30. AU="Perez, Tate"
  31. AU="Bakkaloglu, Sevan"
  32. AU="Guernieri, Rebecca L"
  33. AU="Xing, Z Y"
  34. AU="Yu-Heng Cheng"
  35. AU=Freeman Richard B Jr
  36. AU="Wang, Qi-En"
  37. AU="Mallamaci, M"
  38. AU="Turk, Yael R"
  39. AU="Tinto, Monica"
  40. AU="Selvendiran, Karuppaiyah" AU="Selvendiran, Karuppaiyah"
  41. AU="Enns, Murray W"
  42. AU="Yaohua Yang" AU="Yaohua Yang"

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  1. Artikel ; Online: Non-selective dampening of the host immune response after hepatitis C clearance and its association with circulating chemokine and endotoxin levels.

    Quinn, Gabriella / Ali, Rabab O / Zhang, Grace Y / Hill, Kareen / Townsend, Elizabeth / Umarova, Regina / Chakraborty, Moumita / Ahmad, Maleeha F / Gewirtz, Meital / Haddad, James / Rosenzweig, Sergio / Rampertaap, Shakuntala / Schoenfeld, Megan / Yang, Shanna / Koh, Christopher / Levy, Elliot / Kleiner, David E / Etzion, Ohad / Heller, Theo

    Liver international : official journal of the International Association for the Study of the Liver

    2023  Band 43, Heft 12, Seite(n) 2701–2712

    Abstract: Background & aims: Direct-acting antiviral (DAA) therapy has revolutionized treatment for the hepatitis C virus (HCV). While DAA therapy is common, little is known about the intrahepatic immunological changes after sustained virologic response (SVR). We ...

    Abstract Background & aims: Direct-acting antiviral (DAA) therapy has revolutionized treatment for the hepatitis C virus (HCV). While DAA therapy is common, little is known about the intrahepatic immunological changes after sustained virologic response (SVR). We aim to describe transcriptional alterations of the gut microbiome and the liver after SVR.
    Methods: Twenty-two HCV patients were evaluated before and 9 months after 12 weeks of sofosbuvir/velpatasvir treatment. All achieved SVR. A liver biopsy, portal blood (direct portal vein cannulation), peripheral blood and stool samples were obtained. RNA-seq and immunofluorescent staining were performed on liver biopsies. RNA-seq and 16S rRNA metagenomics were performed on stool.
    Results: Differential expression within liver transcription showed 514 downregulated genes (FDR q < .05; foldchange > 2) enriched in inflammatory pathways; of note, GO:0060337, type 1 IFN signalling (p = 8e-23) and GO:0042742, defence response to bacterium (p = 8e-3). Interestingly, microbial products increased in the portal blood and liver after SVR. Due to the increase in microbial products, the gut microbiome was investigated. There was no dysbiosis by Shannon diversity index or Bacteroides/Firmicutes ratio. There was a differential increase in genes responsible for bacterial lipopolysaccharide production after SVR.
    Conclusions: The decrease in the antiviral interferon pathway expression was expected after SVR; however, there was an unanticipated decrease in the transcription of genes involved in recognition and response to bacteria, which was associated with increased levels of microbial products. Finally, the alterations in the function of the gut microbiome are a promising avenue for further investigation of the gut-liver axis, especially in the context of the significant immunological changes noted after SVR.
    Mesh-Begriff(e) Humans ; Antiviral Agents/therapeutic use ; Hepacivirus ; Hepatitis C, Chronic/complications ; Endotoxins/therapeutic use ; RNA, Ribosomal, 16S/genetics ; Hepatitis C/complications ; Sustained Virologic Response ; Chemokines/therapeutic use ; Immunity
    Chemische Substanzen Antiviral Agents ; Endotoxins ; RNA, Ribosomal, 16S ; Chemokines
    Sprache Englisch
    Erscheinungsdatum 2023-09-26
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Intramural
    ZDB-ID 2102783-3
    ISSN 1478-3231 ; 1478-3223
    ISSN (online) 1478-3231
    ISSN 1478-3223
    DOI 10.1111/liv.15737
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Neonatal exposure to a wild-derived microbiome protects mice against diet-induced obesity.

    Hild, Benedikt / Dreier, Matthew S / Oh, Ji Hoon / McCulloch, John A / Badger, Jonathan H / Guo, Juen / Thefaine, Claire E / Umarova, Regina / Hall, Kevin D / Gavrilova, Oksana / Rosshart, Stephan P / Trinchieri, Giorgio / Rehermann, Barbara

    Nature metabolism

    2021  Band 3, Heft 8, Seite(n) 1042–1057

    Abstract: Obesity and its consequences are among the greatest challenges in healthcare. The gut microbiome is recognized as a key factor in the pathogenesis of obesity. Using a mouse model, we show here that a wild-derived microbiome protects against excessive ... ...

    Abstract Obesity and its consequences are among the greatest challenges in healthcare. The gut microbiome is recognized as a key factor in the pathogenesis of obesity. Using a mouse model, we show here that a wild-derived microbiome protects against excessive weight gain, severe fatty liver disease and metabolic syndrome during a 10-week course of high-fat diet. This phenotype is transferable only during the first weeks of life. In adult mice, neither transfer nor severe disturbance of the wild-type microbiome modifies the metabolic response to a high-fat diet. The protective phenotype is associated with increased secretion of metabolic hormones and increased energy expenditure through activation of brown adipose tissue. Thus, we identify a microbiome that protects against weight gain and its negative consequences through metabolic programming in early life. Translation of these results to humans may identify early-life therapeutics that protect against obesity.
    Mesh-Begriff(e) Animal Feed ; Animals ; Diet/adverse effects ; Diet, High-Fat ; Disease Models, Animal ; Disease Resistance ; Disease Susceptibility ; Energy Metabolism ; Environmental Exposure ; Gastrointestinal Microbiome ; Host Microbial Interactions ; Mice ; Microbiota ; Obesity/etiology ; Time Factors ; Weight Gain
    Sprache Englisch
    Erscheinungsdatum 2021-08-20
    Erscheinungsland Germany
    Dokumenttyp Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-021-00439-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Prospective Study of Withdrawal of Antiviral Therapy in Patients with Chronic Hepatitis B after Prolonged Virological Response.

    Gara, Naveen / Tana, Michele M / Kattapuram, Meera / Auh, Sungyoung / Sullivan, Lauren / Fryzek, Nancy / Walter, Mary / Umarova, Regina / Zhao, Xiongce / Cloherty, Gavin / Doo, Edward / Heller, Theo / Liang, T Jake / Ghany, Marc G

    Hepatology communications

    2021  Band 5, Heft 11, Seite(n) 1888–1900

    Abstract: Nucleoside analogue (NA) therapy for chronic hepatitis B (CHB) is associated with improved clinical outcomes, but usually requires long-term use. Whether treatment can be safely withdrawn and the factors associated with post-withdrawal outcome are not ... ...

    Abstract Nucleoside analogue (NA) therapy for chronic hepatitis B (CHB) is associated with improved clinical outcomes, but usually requires long-term use. Whether treatment can be safely withdrawn and the factors associated with post-withdrawal outcome are not well defined. To assess long-term outcomes after stopping antiviral therapy, patients with hepatitis B e antigen (HBeAg)-negative CHB who had received antiviral therapy for 4 or more years with hepatitis B virus (HBV) DNA (≤100 IU/mL) were prospectively withdrawn from antiviral therapy and monitored monthly for the initial 6 months and every 3 months thereafter. Those with clinical relapse were retreated according to severity of relapse. Fifteen patients were withdrawn from lamivudine (4), adefovir (5), or a combination of the two (6) after a mean treatment duration of 8.4 years. The mean age was 45 years, 13 were male, and 8 were initially HBeAg-positive before treatment. After a mean follow-up of 6.6 years, outcomes differed by pretreatment HBeAg status. All patients who were HBeAg+ before treatment experienced virological relapse (8 of 8); 6 of 8 experienced clinical relapse; 4 of 8 had ALT flares; 5 of 8 required re-initiation of treatment, one of whom cleared hepatitis B surface antigen (HBsAg); and 3 of 8 remained off treatment, one of whom cleared HBsAg. In contrast, 4 of 7 patients who were HBeAg-negative before treatment experienced virological relapse, 3 of 7 experienced clinical relapse, and 1 of 7 had an alanine aminotransferase (ALT) flare. None restarted treatment, and 4 of 7 cleared HBsAg. Low pre-withdrawal HBsAg level was predictive of HBsAg loss. Conclusion: NA therapy can be safely withdrawn with long-term remission and high rates of HBsAg loss in most HBeAg-negative patients without cirrhosis. Patients who were initially HBeAg+ should not be withdrawn from treatment, because clinical relapse was frequent and often severe.
    Mesh-Begriff(e) Adult ; Antiviral Agents/administration & dosage ; DNA, Viral/blood ; Female ; Hepatitis B Surface Antigens/blood ; Hepatitis B Surface Antigens/immunology ; Hepatitis B virus/drug effects ; Hepatitis B, Chronic/blood ; Hepatitis B, Chronic/drug therapy ; Humans ; Induction Chemotherapy ; Male ; Middle Aged ; Pilot Projects ; Prospective Studies ; Recurrence ; Sustained Virologic Response ; Withholding Treatment
    Chemische Substanzen Antiviral Agents ; DNA, Viral ; Hepatitis B Surface Antigens
    Sprache Englisch
    Erscheinungsdatum 2021-08-06
    Erscheinungsland United States
    Dokumenttyp Clinical Trial ; Journal Article ; Research Support, N.I.H., Intramural
    ISSN 2471-254X
    ISSN (online) 2471-254X
    DOI 10.1002/hep4.1761
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: 17-Beta Hydroxysteroid Dehydrogenase 13 Deficiency Does Not Protect Mice From Obesogenic Diet Injury.

    Ma, Yanling / Brown, Philip M / Lin, Dennis D / Ma, Jing / Feng, Dechun / Belyaeva, Olga V / Podszun, Maren C / Roszik, Jason / Allen, Joselyn N / Umarova, Regina / Kleiner, David E / Kedishvili, Natalia Y / Gavrilova, Oksana / Gao, Bin / Rotman, Yaron

    Hepatology (Baltimore, Md.)

    2021  Band 73, Heft 5, Seite(n) 1701–1716

    Abstract: Background and aims: 17-Beta hydroxysteroid dehydrogenase 13 (HSD17B13) is genetically associated with human nonalcoholic fatty liver disease (NAFLD). Inactivating mutations in HSD17B13 protect humans from NAFLD-associated and alcohol-associated liver ... ...

    Abstract Background and aims: 17-Beta hydroxysteroid dehydrogenase 13 (HSD17B13) is genetically associated with human nonalcoholic fatty liver disease (NAFLD). Inactivating mutations in HSD17B13 protect humans from NAFLD-associated and alcohol-associated liver injury, fibrosis, cirrhosis, and hepatocellular carcinoma, leading to clinical trials of anti-HSD17B13 therapeutic agents in humans. We aimed to study the in vivo function of HSD17B13 using a mouse model.
    Approach and results: Single-cell RNA-sequencing and quantitative RT-PCR data revealed that hepatocytes are the main HSD17B13-expressing cells in mice and humans. We compared Hsd17b13 whole-body knockout (KO) mice and wild-type (WT) littermate controls fed regular chow (RC), a high-fat diet (HFD), a Western diet (WD), or the National Institute on Alcohol Abuse and Alcoholism model of alcohol exposure. HFD and WD induced significant weight gain, hepatic steatosis, and inflammation. However, there was no difference between genotypes with regard to body weight, liver weight, hepatic triglycerides (TG), histological inflammatory scores, expression of inflammation-related and fibrosis-related genes, and hepatic retinoid levels. Compared to WT, KO mice on the HFD had hepatic enrichment of most cholesterol esters, monoglycerides, and certain sphingolipid species. Extended feeding with the WD for 10 months led to extensive liver injury, fibrosis, and hepatocellular carcinoma, with no difference between genotypes. Under alcohol exposure, KO and WT mice showed similar hepatic TG and liver enzyme levels. Interestingly, chow-fed KO mice showed significantly higher body and liver weights compared to WT mice, while KO mice on obesogenic diets had a shift toward larger lipid droplets.
    Conclusions: Extensive evaluation of Hsd17b13 deficiency in mice under several fatty liver-inducing dietary conditions did not reproduce the protective role of HSD17B13 loss-of-function mutants in human NAFLD. Moreover, mouse Hsd17b13 deficiency induces weight gain under RC. It is crucial to understand interspecies differences prior to leveraging HSD17B13 therapies.
    Mesh-Begriff(e) 17-Hydroxysteroid Dehydrogenases/deficiency ; 17-Hydroxysteroid Dehydrogenases/metabolism ; Animals ; Diet, High-Fat/adverse effects ; Diet, Western/adverse effects ; Ethanol/adverse effects ; Fatty Liver/etiology ; Lipids/analysis ; Liver/chemistry ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Weight Gain
    Chemische Substanzen Lipids ; Ethanol (3K9958V90M) ; 17-Hydroxysteroid Dehydrogenases (EC 1.1.-) ; 17beta-hydroxysteroid dehydrogenase type 13, mouse (EC 1.1.-)
    Sprache Englisch
    Erscheinungsdatum 2021-03-16
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Intramural
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.31517
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  5. Artikel ; Online: Longitudinal multi-omics analyses of the gut-liver axis reveals metabolic dysregulation in hepatitis C infection and cirrhosis.

    Ali, Rabab O / Quinn, Gabriella M / Umarova, Regina / Haddad, James A / Zhang, Grace Y / Townsend, Elizabeth C / Scheuing, Lisa / Hill, Kareen L / Gewirtz, Meital / Rampertaap, Shakuntala / Rosenzweig, Sergio D / Remaley, Alan T / Han, Jung Min / Periwal, Vipul / Cai, Hongyi / Walter, Peter J / Koh, Christopher / Levy, Elliot B / Kleiner, David E /
    Etzion, Ohad / Heller, Theo

    Nature microbiology

    2022  Band 8, Heft 1, Seite(n) 12–27

    Abstract: The gut and liver are connected via the portal vein, and this relationship, which includes the gut microbiome, is described as the gut-liver axis. Hepatitis C virus (HCV) can infect the liver and cause fibrosis with chronic infection. HCV has been ... ...

    Abstract The gut and liver are connected via the portal vein, and this relationship, which includes the gut microbiome, is described as the gut-liver axis. Hepatitis C virus (HCV) can infect the liver and cause fibrosis with chronic infection. HCV has been associated with an altered gut microbiome; however, how these changes impact metabolism across the gut-liver axis and how this varies with disease severity and time is unclear. Here we used multi-omics analysis of portal and peripheral blood, faeces and liver tissue to characterize the gut-liver axis of patients with HCV across a fibrosis severity gradient before (n = 29) and 6 months after (n = 23) sustained virologic response, that is, no detection of the virus. Fatty acids were the major metabolites perturbed across the liver, portal vein and gut microbiome in HCV, especially in patients with cirrhosis. Decreased fatty acid degradation by hepatic peroxisomes and mitochondria was coupled with increased free fatty acid (FFA) influx to the liver via the portal vein. Metatranscriptomics indicated that Anaerostipes hadrus-mediated fatty acid synthesis influences portal FFAs. Both microbial fatty acid synthesis and portal FFAs were associated with enhanced hepatic fibrosis. Bacteroides vulgatus-mediated intestinal glycan breakdown was linked to portal glycan products, which in turn correlated with enhanced portal inflammation in HCV. Paired comparison of patient samples at both timepoints showed that hepatic metabolism, especially in peroxisomes, is persistently dysregulated in cirrhosis independently of the virus. Sustained virologic response was associated with a potential beneficial role for Methanobrevibacter smithii, which correlated with liver disease severity markers. These results develop our understanding of the gut-liver axis in HCV and non-HCV liver disease aetiologies and provide a foundation for future therapies.
    Mesh-Begriff(e) Humans ; Multiomics ; Liver Cirrhosis ; Hepatitis C/complications ; Hepacivirus/genetics
    Sprache Englisch
    Erscheinungsdatum 2022-12-15
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Intramural
    ISSN 2058-5276
    ISSN (online) 2058-5276
    DOI 10.1038/s41564-022-01273-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Diminished hepatic IFN response following HCV clearance triggers HBV reactivation in coinfection.

    Cheng, Xiaoming / Uchida, Takuro / Xia, Yuchen / Umarova, Regina / Liu, Chun-Jen / Chen, Pei-Jer / Gaggar, Anuj / Suri, Vithika / Mücke, Marcus M / Vermehren, Johannes / Zeuzem, Stefan / Teraoka, Yuji / Osawa, Mitsutaka / Aikata, Hiroshi / Tsuji, Keiji / Mori, Nami / Hige, Shuhei / Karino, Yoshiyasu / Imamura, Michio /
    Chayama, Kazuaki / Liang, T Jake

    The Journal of clinical investigation

    2020  Band 130, Heft 6, Seite(n) 3205–3220

    Abstract: In patients with HBV and HCV coinfection, HBV reactivation leading to severe hepatitis has been reported with the use of direct-acting antivirals (DAAs) to treat HCV infection. Here we studied the molecular mechanisms behind this viral interaction. In ... ...

    Abstract In patients with HBV and HCV coinfection, HBV reactivation leading to severe hepatitis has been reported with the use of direct-acting antivirals (DAAs) to treat HCV infection. Here we studied the molecular mechanisms behind this viral interaction. In coinfected cell culture and humanized mice, HBV replication was suppressed by HCV coinfection. In vitro, HBV suppression was attenuated when interferon (IFN) signaling was blocked. In vivo, HBV viremia, after initial suppression by HCV superinfection, rebounded following HCV clearance by DAA treatment that was accompanied by a reduced hepatic IFN response. Using blood samples of coinfected patients, IFN-stimulated gene products including C-X-C motif chemokine 10 (CXCL10), C-C motif chemokine ligand 5 (CCL5), and alanine aminotransferase (ALT) were identified to have predictive value for HBV reactivation after HCV clearance. Taken together, our data suggest that HBV reactivation is a result of diminished hepatic IFN response following HCV clearance and identify serologic markers that can predict HBV reactivation in DAA-treated HBV-HCV-coinfected persons.
    Mesh-Begriff(e) Animals ; Chemokine CCL5/immunology ; Chemokine CXCL10/immunology ; Coinfection/immunology ; Coinfection/pathology ; Coinfection/virology ; Hepacivirus/physiology ; Hepatitis B/immunology ; Hepatitis B/pathology ; Hepatitis B/virology ; Hepatitis B virus/physiology ; Hepatitis C/immunology ; Hepatitis C/pathology ; Hepatitis C/virology ; Humans ; Interferons/immunology ; Liver/immunology ; Liver/pathology ; Liver/virology ; Mice ; Virus Activation/immunology
    Chemische Substanzen CCL5 protein, human ; CXCL10 protein, human ; Chemokine CCL5 ; Chemokine CXCL10 ; Interferons (9008-11-1)
    Sprache Englisch
    Erscheinungsdatum 2020-03-12
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI135616
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Vitamin E treatment in NAFLD patients demonstrates that oxidative stress drives steatosis through upregulation of de-novo lipogenesis.

    Podszun, Maren C / Alawad, Ahmad S / Lingala, Shilpa / Morris, Nevitt / Huang, Wen-Chun A / Yang, Shanna / Schoenfeld, Megan / Rolt, Adam / Ouwerkerk, Ronald / Valdez, Kristin / Umarova, Regina / Ma, Yanling / Fatima, Syeda Zaheen / Lin, Dennis D / Mahajan, Lakshmi S / Samala, Niharika / Violet, Pierre-Christian / Levine, Mark / Shamburek, Robert /
    Gharib, Ahmed M / Kleiner, David E / Garraffo, H Martin / Cai, Hongyi / Walter, Peter J / Rotman, Yaron

    Redox biology

    2020  Band 37, Seite(n) 101710

    Abstract: Oxidative stress (OS) in non-alcoholic fatty liver disease (NAFLD) promotes liver injury and inflammation. Treatment with vitamin E (α-tocopherol, αT), a lipid-soluble antioxidant, improves liver injury but also decreases steatosis, thought to be ... ...

    Abstract Oxidative stress (OS) in non-alcoholic fatty liver disease (NAFLD) promotes liver injury and inflammation. Treatment with vitamin E (α-tocopherol, αT), a lipid-soluble antioxidant, improves liver injury but also decreases steatosis, thought to be upstream of OS, through an unknown mechanism. To elucidate the mechanism, we combined a mechanistic human trial interrogating pathways of intrahepatic triglyceride (IHTG) accumulation and in vitro experiments. 50% of NAFLD patients (n = 20) treated with αT (200-800 IU/d) for 24 weeks had a ≥ 25% relative decrease in IHTG by magnetic resonance spectroscopy. Paired liver biopsies at baseline and week 4 of treatment revealed a decrease in markers of hepatic de novo lipogenesis (DNL) that strongly predicted week 24 response. In vitro, using HepG2 cells and primary human hepatocytes, αT inhibited glucose-induced DNL by decreasing SREBP-1 processing and lipogenic gene expression. This mechanism is dependent on the antioxidant capacity of αT, as redox-silenced methoxy-αT is unable to inhibit DNL in vitro. OS by itself was sufficient to increase S2P expression in vitro, and S2P is upregulated in NAFLD livers. In summary, we utilized αT to demonstrate a vicious cycle in which NAFLD generates OS, which feeds back to augment DNL and increases steatosis. Clinicaltrials.gov: NCT01792115.
    Mesh-Begriff(e) Humans ; Lipogenesis ; Liver/metabolism ; Non-alcoholic Fatty Liver Disease/drug therapy ; Non-alcoholic Fatty Liver Disease/metabolism ; Oxidative Stress ; Up-Regulation ; Vitamin E/metabolism ; Vitamin E/pharmacology
    Chemische Substanzen Vitamin E (1406-18-4)
    Sprache Englisch
    Erscheinungsdatum 2020-09-01
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2020.101710
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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