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  1. Article ; Online: Tumorigenesis from non-alcoholic steatohepatitis to hepatocellular carcinoma.

    Yu, Junjie / Pajvani, Utpal B

    Medical review (2021)

    2023  Volume 2, Issue 6, Page(s) 544–546

    Abstract: Non-alcoholic steatohepatitis (NASH) with metabolic syndrome is increasing to be a main cause of hepatocellular carcinoma (HCC). However, the mechanism of tumorigenesis in NASH induced HCC is still not clear. In this perspective, we will discuss the ... ...

    Abstract Non-alcoholic steatohepatitis (NASH) with metabolic syndrome is increasing to be a main cause of hepatocellular carcinoma (HCC). However, the mechanism of tumorigenesis in NASH induced HCC is still not clear. In this perspective, we will discuss the recent progress that has been made to understand the genetic change and the immune microenvironment of HCC, and the remaining questions. Based on the current study, NASH-HCC is likely to have novel mechanism, which needs more investigation in future.
    Language English
    Publishing date 2023-01-06
    Publishing country Germany
    Document type Journal Article
    ISSN 2749-9642
    ISSN (online) 2749-9642
    DOI 10.1515/mr-2022-0043
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Tumorigenesis from non-alcoholic steatohepatitis to hepatocellular carcinoma

    Yu Junjie / Pajvani Utpal B.

    Medical Review, Vol 2, Iss 6, Pp 544-

    2023  Volume 546

    Abstract: Non-alcoholic steatohepatitis (NASH) with metabolic syndrome is increasing to be a main cause of hepatocellular carcinoma (HCC). However, the mechanism of tumorigenesis in NASH induced HCC is still not clear. In this perspective, we will discuss the ... ...

    Abstract Non-alcoholic steatohepatitis (NASH) with metabolic syndrome is increasing to be a main cause of hepatocellular carcinoma (HCC). However, the mechanism of tumorigenesis in NASH induced HCC is still not clear. In this perspective, we will discuss the recent progress that has been made to understand the genetic change and the immune microenvironment of HCC, and the remaining questions. Based on the current study, NASH-HCC is likely to have novel mechanism, which needs more investigation in future.
    Keywords hepatocellular carcinoma ; non-alcoholic steatohepatitis ; tumorigenesis ; Medicine ; R
    Language English
    Publishing date 2023-01-01T00:00:00Z
    Publisher De Gruyter
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Integrating stress signals-XBP1 as a novel mediator of intercellular crosstalk in non-alcoholic steatohepatitis.

    Yu, Junjie / Pajvani, Utpal B

    Translational gastroenterology and hepatology

    2022  Volume 8, Page(s) 13

    Language English
    Publishing date 2022-09-07
    Publishing country China
    Document type Editorial ; Comment
    ISSN 2415-1289
    ISSN (online) 2415-1289
    DOI 10.21037/tgh-22-73
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Protective hepatocyte signals restrain liver fibrosis in metabolic dysfunction-associated steatohepatitis.

    Steffani, Marcella / Geng, Yana / Pajvani, Utpal B / Schwabe, Robert F

    The Journal of clinical investigation

    2024  Volume 134, Issue 7

    Abstract: Metabolic dysfunction-associated steatotic liver disease (MASLD) affects nearly 40% of the global adult population and may progress to metabolic dysfunction-associated steatohepatitis (MASH), and MASH-associated liver fibrosis and cirrhosis. Despite ... ...

    Abstract Metabolic dysfunction-associated steatotic liver disease (MASLD) affects nearly 40% of the global adult population and may progress to metabolic dysfunction-associated steatohepatitis (MASH), and MASH-associated liver fibrosis and cirrhosis. Despite numerous studies unraveling the mechanism of hepatic fibrogenesis, there are still no approved antifibrotic therapies. The development of MASLD and liver fibrosis results from complex cell-cell interactions that often initiate within hepatocytes but remain incompletely understood. In this issue of the JCI, Yan and colleagues describe an ATF3/HES1/CEBPA/OPN pathway that links hepatocyte signals to fibrogenic activation of hepatic stellate cells and may provide new perspectives on therapeutic options for MASLD-induced liver fibrosis.
    MeSH term(s) Adult ; Humans ; Liver Cirrhosis ; Hepatocytes ; Fatty Liver ; Hepatic Stellate Cells ; Cell Communication
    Language English
    Publishing date 2024-04-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI179710
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Liver insulinization as a driver of triglyceride dysmetabolism.

    Cook, Joshua R / Hawkins, Meredith A / Pajvani, Utpal B

    Nature metabolism

    2023  Volume 5, Issue 7, Page(s) 1101–1110

    Abstract: Metabolic dysfunction-associated fatty liver disease (MAFLD) is an increasingly prevalent fellow traveller with the insulin resistance that underlies type 2 diabetes mellitus. However, the mechanistic connection between MAFLD and impaired insulin action ... ...

    Abstract Metabolic dysfunction-associated fatty liver disease (MAFLD) is an increasingly prevalent fellow traveller with the insulin resistance that underlies type 2 diabetes mellitus. However, the mechanistic connection between MAFLD and impaired insulin action remains unclear. In this Perspective, we review data from humans to elucidate insulin's aetiological role in MAFLD. We focus particularly on the relative preservation of insulin's stimulation of triglyceride (TG) biosynthesis despite its waning ability to curb hepatic glucose production (HGP). To explain this apparent 'selective insulin resistance', we propose that hepatocellular processes that lead to TG accumulation require less insulin signal transduction, or 'insulinization,' than do those that regulate HGP. As such, mounting hyperinsulinaemia that barely compensates for aberrant HGP in insulin-resistant states more than suffices to maintain hepatic TG biosynthesis. Thus, even modestly elevated or context-inappropriate insulin levels, when sustained day and night within a heavily pro-lipogenic metabolic milieu, may translate into substantial cumulative TG biosynthesis in the insulin-resistant state.
    MeSH term(s) Humans ; Insulin Resistance ; Triglycerides/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Insulin/metabolism ; Glucose/metabolism ; Liver/metabolism
    Chemical Substances Triglycerides ; Insulin ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2023-07-17
    Publishing country Germany
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-023-00843-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: An Ultradian Notch in Beta-Cell Development.

    Pajvani, Utpal B / Sussel, Lori

    The New England journal of medicine

    2020  Volume 383, Issue 1, Page(s) 80–82

    MeSH term(s) Cell Differentiation ; Organogenesis ; Pancreas ; Signal Transduction
    Language English
    Publishing date 2020-07-01
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMcibr2001628
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    Ua VI Zs.34: Show issues Location:
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  7. Article ; Online: MTOR and Beta Cell Adaptation in T2D.

    Bartolomé, Alberto / Pajvani, Utpal B

    The Journal of clinical endocrinology and metabolism

    2020  Volume 106, Issue 3, Page(s) e1466–e1467

    MeSH term(s) Diabetes Mellitus, Type 2/metabolism ; Humans ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; TOR Serine-Threonine Kinases/metabolism
    Chemical Substances MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2020-12-03
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 3029-6
    ISSN 1945-7197 ; 0021-972X
    ISSN (online) 1945-7197
    ISSN 0021-972X
    DOI 10.1210/clinem/dgaa906
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    Uh III Zs.134: Show issues Location:
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  8. Article ; Online: The first MASH drug therapy on the horizon: Current perspectives of resmetirom.

    Petta, Salvatore / Targher, Giovanni / Romeo, Stefano / Pajvani, Utpal B / Zheng, Ming-Hua / Aghemo, Alessio / Valenti, Luca V C

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

    2024  

    Abstract: The rising prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) poses a significant global health challenge, affecting over 30% of adults worldwide. MASLD is linked to increased mortality rates and substantial healthcare costs, ... ...

    Abstract The rising prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) poses a significant global health challenge, affecting over 30% of adults worldwide. MASLD is linked to increased mortality rates and substantial healthcare costs, primarily driven by its progression to metabolic dysfunction-associated steatohepatitis (MASH), which can lead to severe liver complications including cirrhosis and hepatocellular carcinoma. Despite its growing burden, effective pharmacotherapy for MASLD/MASH has been lacking until the recent conditional approval of resmetirom by the FDA. Resmetirom, a liver-targeted thyroid hormone receptor-β selective drug, has shown promise in clinical trials for treating non-cirrhotic MASH with moderate to advanced fibrosis. It has demonstrated efficacy in reducing hepatic fat content, improving liver histology (both MASH resolution and fibrosis improvement), and ameliorating biomarkers of liver damage without significant effects on body weight or glucose metabolism. Notably, resmetirom also exhibits favourable effects on circulating lipids, potentially reducing cardiovascular risk in MASLD/MASH patients. The safety profile of resmetirom appears acceptable, with gastrointestinal adverse events being the most common, though generally mild or moderate. However, long-term surveillance is warranted to monitor for potential risks related to thyroid, gonadal, or bone diseases. Clinical implementation of resmetirom faces challenges in patient selection and monitoring treatment response, and will heavily rely on non-invasive tests for liver fibrosis assessment. Nonetheless, resmetirom represents a landmark breakthrough in MASLD/MASH treatment, paving the way for future therapeutic strategies aiming to mitigate the multifaceted risks associated with this complex metabolic liver disease.
    Language English
    Publishing date 2024-04-05
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2102783-3
    ISSN 1478-3231 ; 1478-3223
    ISSN (online) 1478-3231
    ISSN 1478-3223
    DOI 10.1111/liv.15930
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  9. Article ; Online: Author Correction: Inhibition of Notch signaling ameliorates insulin resistance in a FoxO1-dependent manner.

    Pajvani, Utpal B / Shawber, Carrie J / Samuel, Varman T / Birkenfeld, Andreas L / Shulman, Gerald I / Kitajewski, Jan / Accili, Domenico

    Nature medicine

    2023  Volume 30, Issue 2, Page(s) 604

    Language English
    Publishing date 2023-12-02
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/s41591-023-02695-9
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    Zs.A 4212: Show issues Location:
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  10. Article ; Online: MafA Regulation in β-Cells: From Transcriptional to Post-Translational Mechanisms.

    Liang, Jiani / Chirikjian, Margot / Pajvani, Utpal B / Bartolomé, Alberto

    Biomolecules

    2022  Volume 12, Issue 4

    Abstract: β-cells are insulin-producing cells in the pancreas that maintain euglycemic conditions. Pancreatic β-cell maturity and function are regulated by a variety of transcription factors that enable the adequate expression of the cellular machinery involved in ...

    Abstract β-cells are insulin-producing cells in the pancreas that maintain euglycemic conditions. Pancreatic β-cell maturity and function are regulated by a variety of transcription factors that enable the adequate expression of the cellular machinery involved in nutrient sensing and commensurate insulin secretion. One of the key factors in this regulation is MAF bZIP transcription factor A (MafA). MafA expression is decreased in type 2 diabetes, contributing to β-cell dysfunction and disease progression. The molecular biology underlying MafA is complex, with numerous transcriptional and post-translational regulatory nodes. Understanding these complexities may uncover potential therapeutic targets to ameliorate β-cell dysfunction. This article will summarize the role of MafA in normal β-cell function and disease, with a special focus on known transcriptional and post-translational regulators of MafA expression.
    MeSH term(s) Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Humans ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Maf Transcription Factors, Large/genetics ; Maf Transcription Factors, Large/metabolism
    Chemical Substances Insulin ; Maf Transcription Factors, Large
    Language English
    Publishing date 2022-03-31
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2701262-1
    ISSN 2218-273X ; 2218-273X
    ISSN (online) 2218-273X
    ISSN 2218-273X
    DOI 10.3390/biom12040535
    Database MEDical Literature Analysis and Retrieval System OnLINE

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