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  1. Article ; Online: Reprogramming of Hepatic Metabolism and Microenvironment in Nonalcoholic Steatohepatitis.

    Rui, Liangyou / Lin, Jiandie D

    Annual review of nutrition

    2022  Volume 42, Page(s) 91–113

    Abstract: Nonalcoholic fatty liver disease (NAFLD), a spectrum of metabolic liver disease associated with obesity, ranges from relatively benign hepatic steatosis to nonalcoholic steatohepatitis (NASH). The latter is characterized by persistent liver injury, ... ...

    Abstract Nonalcoholic fatty liver disease (NAFLD), a spectrum of metabolic liver disease associated with obesity, ranges from relatively benign hepatic steatosis to nonalcoholic steatohepatitis (NASH). The latter is characterized by persistent liver injury, inflammation, and liver fibrosis, which collectively increase the risk for end-stage liver diseases such as cirrhosis and hepatocellular carcinoma. Recent work has shed new light on the pathophysiology of NAFLD/NASH, particularly the role of genetic, epigenetic, and dietary factors and metabolic dysfunctions in other tissues in driving excess hepatic fat accumulation and liver injury. In parallel, single-cell RNA sequencing studies have revealed unprecedented details of the molecular nature of liver cell heterogeneity, intrahepatic cross talk, and disease-associated reprogramming of the liver immune and stromal vascular microenvironment. This review covers the recent advances in these areas, the emerging concepts of NASH pathogenesis, and potential new therapeutic opportunities.
    MeSH term(s) Carcinoma, Hepatocellular/complications ; Carcinoma, Hepatocellular/pathology ; Humans ; Liver/metabolism ; Liver Cirrhosis/complications ; Liver Cirrhosis/pathology ; Liver Neoplasms/complications ; Liver Neoplasms/genetics ; Liver Neoplasms/pathology ; Non-alcoholic Fatty Liver Disease/metabolism ; Tumor Microenvironment
    Language English
    Publishing date 2022-05-18
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 406980-8
    ISSN 1545-4312 ; 0199-9885
    ISSN (online) 1545-4312
    ISSN 0199-9885
    DOI 10.1146/annurev-nutr-062220-105200
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1786: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  2. Article ; Online: GPNMB: expanding the code for liver-fat communication.

    Kuang, Henry / Lin, Jiandie D

    Nature metabolism

    2019  Volume 1, Issue 5, Page(s) 507–508

    Language English
    Publishing date 2019-10-14
    Publishing country Germany
    Document type Journal Article
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-019-0069-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Neuregulin 4 mediates the metabolic benefits of mild cold exposure by promoting beige fat thermogenesis.

    Chen, Zhimin / Zhang, Peng / Liu, Tongyu / Qiu, Xiaoxue / Li, Siming / Lin, Jiandie D

    JCI insight

    2024  Volume 9, Issue 1

    Abstract: Interorgan crosstalk via secreted hormones and metabolites is a fundamental aspect of mammalian metabolic physiology. Beyond the highly specialized endocrine cells, peripheral tissues are emerging as an important source of metabolic hormones that ... ...

    Abstract Interorgan crosstalk via secreted hormones and metabolites is a fundamental aspect of mammalian metabolic physiology. Beyond the highly specialized endocrine cells, peripheral tissues are emerging as an important source of metabolic hormones that influence energy and nutrient metabolism and contribute to disease pathogenesis. Neuregulin 4 (Nrg4) is a fat-derived hormone that protects mice from nonalcoholic steatohepatitis (NASH) and NASH-associated liver cancer by shaping hepatic lipid metabolism and the liver immune microenvironment. Despite its enriched expression in brown fat, whether NRG4 plays a role in thermogenic response and mediates the metabolic benefits of cold exposure are areas that remain unexplored. Here we show that Nrg4 expression in inguinal white adipose tissue (iWAT) is highly responsive to chronic cold exposure. Nrg4 deficiency impairs beige fat induction and renders mice more susceptible to diet-induced metabolic disorders under mild cold conditions. Using mice with adipocyte and hepatocyte-specific Nrg4 deletion, we reveal that adipose tissue-derived NRG4, but not hepatic NRG4, is essential for beige fat induction following cold acclimation. Furthermore, treatment with recombinant NRG4-Fc fusion protein promotes beige fat induction in iWAT and improves metabolic health in mice with diet-induced obesity. These findings highlight a critical role of NRG4 in mediating beige fat induction and preserving metabolic health under mild cold conditions.
    MeSH term(s) Animals ; Mice ; Adipose Tissue, Beige/metabolism ; Adipose Tissue, Brown/metabolism ; Hormones ; Mammals ; Neuregulins/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; Thermogenesis
    Chemical Substances Hormones ; Neuregulins ; neuregulin-4
    Language English
    Publishing date 2024-01-09
    Publishing country United States
    Document type Journal Article
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.172957
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Functional overlap between the mammalian

    Tang, Vi T / Xiang, Jie / Chen, Zhimin / McCormick, Joseph / Abbineni, Prabhodh S / Chen, Xiao-Wei / Hoenerhoff, Mark / Emmer, Brian T / Khoriaty, Rami / Lin, Jiandie D / Ginsburg, David

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Proteins carrying a signal peptide and/or a transmembrane domain enter the intracellular secretory pathway at the endoplasmic reticulum (ER) and are transported to the Golgi apparatus via COPII vesicles or tubules. SAR1 initiates COPII coat assembly by ... ...

    Abstract Proteins carrying a signal peptide and/or a transmembrane domain enter the intracellular secretory pathway at the endoplasmic reticulum (ER) and are transported to the Golgi apparatus via COPII vesicles or tubules. SAR1 initiates COPII coat assembly by recruiting other coat proteins to the ER membrane. Mammalian genomes encode two
    Language English
    Publishing date 2024-02-29
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.02.27.582310
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Function and Mechanism of Long Noncoding RNAs in Adipocyte Biology.

    Sun, Lei / Lin, Jiandie D

    Diabetes

    2019  Volume 68, Issue 5, Page(s) 887–896

    Abstract: The last two decades have witnessed an explosion of interest in adipocyte biology, coinciding with the upsurge of obesity and metabolic syndrome. Now we have new perspectives on the distinct developmental origins of white, brown, and beige adipocytes and ...

    Abstract The last two decades have witnessed an explosion of interest in adipocyte biology, coinciding with the upsurge of obesity and metabolic syndrome. Now we have new perspectives on the distinct developmental origins of white, brown, and beige adipocytes and their role in metabolic physiology and disease. Beyond fuel metabolism, adipocytes communicate with the immune system and other tissues by releasing diverse paracrine and endocrine factors to orchestrate adipose tissue remodeling and maintain systemic homeostasis. Significant progress has been made in delineating the regulatory networks that govern different aspects of adipocyte biology. Here we provide an overview on the emerging role of long noncoding RNAs (lncRNAs) in the regulation of adipocyte development and metabolism and discuss the implications of the RNA-protein regulatory interface in metabolic control.
    MeSH term(s) Adipocytes/metabolism ; Adipose Tissue/metabolism ; Animals ; Humans ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism
    Chemical Substances RNA, Long Noncoding
    Language English
    Publishing date 2019-04-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/dbi18-0009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uh III Zs.175: Show issues Location:
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  6. Article ; Online: Functional overlap between the mammalian

    Tang, Vi T / Xiang, Jie / Chen, Zhimin / McCormick, Joseph / Abbineni, Prabhodh S / Chen, Xiao-Wei / Hoenerhoff, Mark / Emmer, Brian T / Khoriaty, Rami / Lin, Jiandie D / Ginsburg, David

    Proceedings of the National Academy of Sciences of the United States of America

    2024  Volume 121, Issue 19, Page(s) e2322164121

    Abstract: Proteins carrying a signal peptide and/or a transmembrane domain enter the intracellular secretory pathway at the endoplasmic reticulum (ER) and are transported to the Golgi apparatus via COPII vesicles or tubules. SAR1 initiates COPII coat assembly by ... ...

    Abstract Proteins carrying a signal peptide and/or a transmembrane domain enter the intracellular secretory pathway at the endoplasmic reticulum (ER) and are transported to the Golgi apparatus via COPII vesicles or tubules. SAR1 initiates COPII coat assembly by recruiting other coat proteins to the ER membrane. Mammalian genomes encode two
    MeSH term(s) Animals ; Humans ; Mice ; COP-Coated Vesicles/metabolism ; COP-Coated Vesicles/genetics ; Endoplasmic Reticulum/metabolism ; Hepatocytes/metabolism ; Mice, Knockout ; Monomeric GTP-Binding Proteins/metabolism ; Monomeric GTP-Binding Proteins/genetics
    Chemical Substances Monomeric GTP-Binding Proteins (EC 3.6.5.2) ; SAR1A protein, human (EC 3.6.1.-) ; SAR1B protein, human (EC 3.6.1.-) ; Sar1b protein, mouse (EC 3.6.5.2) ; SARA protein, mouse
    Language English
    Publishing date 2024-04-30
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2322164121
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1148: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  7. Article ; Online: The hepatokine TSK maintains myofiber integrity and exercise endurance and contributes to muscle regeneration

    Qiuyu Wang / Xiaoxue Qiu / Tongyu Liu / Cheehoon Ahn / Jeffrey F. Horowitz / Jiandie D. Lin

    JCI Insight, Vol 7, Iss

    2022  Volume 4

    Abstract: Mammalian skeletal muscle contains heterogenous myofibers with different contractile and metabolic properties that sustain muscle mass and endurance capacity. The transcriptional regulators that govern these myofiber gene programs have been elucidated. ... ...

    Abstract Mammalian skeletal muscle contains heterogenous myofibers with different contractile and metabolic properties that sustain muscle mass and endurance capacity. The transcriptional regulators that govern these myofiber gene programs have been elucidated. However, the hormonal cues that direct the specification of myofiber types and muscle endurance remain largely unknown. Here, we uncover the secreted factor Tsukushi (TSK) as an extracellular signal that is required for maintaining muscle mass, strength, and endurance capacity and that contributes to muscle regeneration. Mice lacking TSK exhibited reduced grip strength and impaired exercise capacity. Muscle transcriptomic analysis revealed that TSK deficiency results in a remarkably selective impairment in the expression of myofibrillar genes, characteristic of slow-twitch muscle fibers, that is associated with abnormal neuromuscular junction formation. AAV-mediated overexpression of TSK failed to rescue these myofiber defects in adult mice, suggesting that the effects of TSK on myofibers are likely restricted to certain developmental stages. Finally, mice lacking TSK exhibited diminished muscle regeneration following cardiotoxin-induced muscle injury. These findings support a crucial role of TSK as a hormonal cue in the regulation of contractile gene expression, endurance capacity, and muscle regeneration.
    Keywords Muscle biology ; Medicine ; R
    Subject code 796
    Language English
    Publishing date 2022-02-01T00:00:00Z
    Publisher American Society for Clinical investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: A Single-Cell Perspective of the Mammalian Liver in Health and Disease.

    Xiong, Xuelian / Kuang, Henry / Liu, Tongyu / Lin, Jiandie D

    Hepatology (Baltimore, Md.)

    2020  Volume 71, Issue 4, Page(s) 1467–1473

    MeSH term(s) Animals ; Cell Communication ; Cellular Reprogramming/genetics ; Humans ; Liver/cytology ; Liver/metabolism ; Liver Diseases/genetics ; Liver Diseases/metabolism ; Liver Diseases/pathology ; Mice ; RNA-Seq ; Single-Cell Analysis
    Language English
    Publishing date 2020-01-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.31149
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    Zs.A 1660: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  9. Article ; Online: Myeloid-specific ablation of Basp1 ameliorates diet-induced NASH in mice by attenuating pro-inflammatory signaling.

    Meng, Ziyi / Zhou, Linkang / Hong, Sungki / Qiu, Xiaoxue / Chen, Zhimin / Liu, Tongyu / Inoki, Ken / Lin, Jiandie D

    Hepatology (Baltimore, Md.)

    2023  Volume 79, Issue 2, Page(s) 409–424

    Abstract: Background and aims: NASH represents a severe stage of fatty liver disease characterized by hepatocyte injury, inflammation, and liver fibrosis. Myeloid-derived innate immune cells, such as macrophages and dendritic cells, play an important role in host ...

    Abstract Background and aims: NASH represents a severe stage of fatty liver disease characterized by hepatocyte injury, inflammation, and liver fibrosis. Myeloid-derived innate immune cells, such as macrophages and dendritic cells, play an important role in host defense and disease pathogenesis. Despite this, the nature of transcriptomic reprogramming of myeloid cells in NASH liver and its contribution to disease progression remain incompletely defined.
    Approach and results: In this study, we performed bulk and single-cell RNA sequencing (sc-RNA seq) analysis to delineate the landscape of macrophage and dendritic cell transcriptomes in healthy and NASH livers. Our analysis uncovered cell type-specific patterns of transcriptomic reprogramming on diet-induced NASH. We identified brain-abundant membrane-attached signal protein 1 (Basp1) as a myeloid-enriched gene that is markedly induced in mouse and human NASH liver. Myeloid-specific inactivation of Basp1 attenuates the severity of diet-induced NASH pathologies, as shown by reduced hepatocyte injury and liver fibrosis in mice. Mechanistically, cultured macrophages lacking Basp1 exhibited a diminished response to pro-inflammatory stimuli, impaired NLRP3 inflammasome activation, and reduced cytokine secretion.
    Conclusions: Together, these findings uncover Basp1 as a critical regulator of myeloid inflammatory signaling that underlies NASH pathogenesis.
    MeSH term(s) Mice ; Humans ; Animals ; Non-alcoholic Fatty Liver Disease/pathology ; Liver/pathology ; Hepatocytes/metabolism ; Diet ; Liver Cirrhosis/pathology ; Mice, Inbred C57BL ; Disease Models, Animal
    Language English
    Publishing date 2023-07-17
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1097/HEP.0000000000000537
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1660: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  10. Article ; Online: The hepatokine TSK maintains myofiber integrity and exercise endurance and contributes to muscle regeneration.

    Wang, Qiuyu / Qiu, Xiaoxue / Liu, Tongyu / Ahn, Cheehoon / Horowitz, Jeffrey F / Lin, Jiandie D

    JCI insight

    2022  Volume 7, Issue 4

    Abstract: Mammalian skeletal muscle contains heterogenous myofibers with different contractile and metabolic properties that sustain muscle mass and endurance capacity. The transcriptional regulators that govern these myofiber gene programs have been elucidated. ... ...

    Abstract Mammalian skeletal muscle contains heterogenous myofibers with different contractile and metabolic properties that sustain muscle mass and endurance capacity. The transcriptional regulators that govern these myofiber gene programs have been elucidated. However, the hormonal cues that direct the specification of myofiber types and muscle endurance remain largely unknown. Here, we uncover the secreted factor Tsukushi (TSK) as an extracellular signal that is required for maintaining muscle mass, strength, and endurance capacity and that contributes to muscle regeneration. Mice lacking TSK exhibited reduced grip strength and impaired exercise capacity. Muscle transcriptomic analysis revealed that TSK deficiency results in a remarkably selective impairment in the expression of myofibrillar genes, characteristic of slow-twitch muscle fibers, that is associated with abnormal neuromuscular junction formation. AAV-mediated overexpression of TSK failed to rescue these myofiber defects in adult mice, suggesting that the effects of TSK on myofibers are likely restricted to certain developmental stages. Finally, mice lacking TSK exhibited diminished muscle regeneration following cardiotoxin-induced muscle injury. These findings support a crucial role of TSK as a hormonal cue in the regulation of contractile gene expression, endurance capacity, and muscle regeneration.
    MeSH term(s) Animals ; Mice ; Mice, Transgenic ; Models, Animal ; Muscle Contraction/physiology ; Muscle Fibers, Slow-Twitch/metabolism ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/physiopathology ; Proteoglycans/biosynthesis ; Proteoglycans/genetics ; Regeneration ; Transcription Factors
    Chemical Substances Proteoglycans ; Transcription Factors ; tsukushi protein, mouse
    Language English
    Publishing date 2022-02-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.154746
    Database MEDical Literature Analysis and Retrieval System OnLINE

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