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  1. Article ; Online: IRGM1 supports host defense against intracellular bacteria through suppression of type I interferon in mice.

    Rai, Prashant / Sharpe, Martin / Ganta, Charan K / Baker, Paul J / Mayer-Barber, Katrin D / Fee, Brian E / Taylor, Gregory A / Fessler, Michael B

    The Journal of clinical investigation

    2023  Volume 133, Issue 21

    MeSH term(s) Animals ; Mice ; Bacteria ; Immunity, Innate ; Interferon Type I ; Macrophages/microbiology
    Chemical Substances Interferon Type I ; Ifi1 protein, mouse
    Language English
    Publishing date 2023-11-01
    Publishing country United States
    Document type Letter
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI171982
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.184: Show issues Location:
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  2. Article ; Online: Enhancing Hepatic MBOAT7 Expression in Mice With Nonalcoholic Steatohepatitis.

    Sharpe, Martin C / Pyles, Kelly D / Hallcox, Taylor / Kamm, Dakota R / Piechowski, Michaela / Fisk, Bryan / Albert, Carolyn J / Carpenter, Danielle H / Ulmasov, Barbara / Ford, David A / Neuschwander-Tetri, Brent A / McCommis, Kyle S

    Gastro hep advances

    2023  Volume 2, Issue 4, Page(s) 558–572

    Abstract: Background and aims: Polymorphisms near the membrane bound O-acyltransferase domain containing 7 (MBOAT7) genes are associated with worsened nonalcoholic fatty liver (NASH), and nonalcoholic fatty liver disease (NAFLD)/NASH may decrease MBOAT7 ... ...

    Abstract Background and aims: Polymorphisms near the membrane bound O-acyltransferase domain containing 7 (MBOAT7) genes are associated with worsened nonalcoholic fatty liver (NASH), and nonalcoholic fatty liver disease (NAFLD)/NASH may decrease MBOAT7 expression independent of these polymorphisms. We hypothesized that enhancing MBOAT7 function would improve NASH.
    Methods: Genomic and lipidomic databases were mined for MBOAT7 expression and hepatic phosphatidylinositol (PI) abundance in human NAFLD/NASH. Male C57BL6/J mice were fed either choline-deficient high-fat diet or Gubra Amylin NASH diet and subsequently infected with adeno-associated virus expressing MBOAT7 or control virus. NASH histological scoring and lipidomic analyses were performed to assess MBOAT7 activity, hepatic PI, and lysophosphatidylinositol (LPI) abundance.
    Results: Human NAFLD/NASH decreases MBOAT7 expression and hepatic abundance of arachidonate-containing PI. Murine NASH models display subtle changes in MBOAT7 expression, but significantly decreased activity. After MBOAT7 overexpression, liver weights, triglycerides, and plasma alanine and aspartate transaminase were modestly improved by MBOAT7 overexpression, but NASH histology was not improved. Despite confirmation of increased activity with MBOAT7 overexpression, content of the main arachidonoylated PI species was not rescued by MBOAT7 although the abundance of many PI species was increased. Free arachidonic acid was elevated but the MBOAT7 substrate arachidonoyl-CoA was decreased in NASH livers compared to low-fat controls, likely due to the decreased expression of long-chain acyl-CoA synthetases.
    Conclusion: Results suggest decreased MBOAT7 activity plays a role in NASH, but MBOAT7 overexpression fails to measurably improve NASH pathology potentially due to the insufficient abundance of its arachidonoyl-CoA substrate.
    Language English
    Publishing date 2023-02-23
    Publishing country Netherlands
    Document type Journal Article
    ISSN 2772-5723
    ISSN (online) 2772-5723
    DOI 10.1016/j.gastha.2023.02.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Novel insulin sensitizer MSDC-0602K improves insulinemia and fatty liver disease in mice, alone and in combination with liraglutide.

    Kamm, Dakota R / Pyles, Kelly D / Sharpe, Martin C / Healy, Laura N / Colca, Jerry R / McCommis, Kyle S

    The Journal of biological chemistry

    2021  Volume 296, Page(s) 100807

    Abstract: Insulin sensitizers and incretin mimetics are antidiabetic agents with vastly different mechanisms of action. Thiazolidinedione (TZD) insulin sensitizers are associated with weight gain, whereas glucagon-like peptide-1 receptor agonists can induce weight ...

    Abstract Insulin sensitizers and incretin mimetics are antidiabetic agents with vastly different mechanisms of action. Thiazolidinedione (TZD) insulin sensitizers are associated with weight gain, whereas glucagon-like peptide-1 receptor agonists can induce weight loss. We hypothesized that combination of a TZD insulin sensitizer and the glucagon-like peptide-1 receptor agonist liraglutide would more significantly improve mouse models of diabetes and nonalcoholic steatohepatitis (NASH). Diabetic db/db and MS-NASH mice were treated with the TZD MSDC-0602K by oral gavage, liraglutide (Lira) by s.c. injection, or combination 0602K+Lira. Lira slightly reduced body weight and modestly improved glycemia in db/db mice. Comparatively, 0602K-treated and 0602K+Lira-treated mice exhibited slight weight gain but completely corrected glycemia and improved glucose tolerance. 0602K reduced plasma insulin, whereas Lira further increased the hyperinsulinemia of db/db mice. Surprisingly, 0602K+Lira treatment reduced plasma insulin and C-peptide to the same extent as mice treated with 0602K alone. 0602K did not reduce glucose-stimulated insulin secretion in vivo, or in isolated islets, indicating the reduced insulinemia was likely compensatory to improved insulin sensitivity. In MS-NASH mice, both 0602K or Lira alone improved plasma alanine aminotransferase and aspartate aminotransferase, as well as liver histology, but more significant improvements were observed with 0602K+Lira treatment. 0602K or 0602K+Lira also increased pancreatic insulin content in both db/db and MS-NASH mice. In conclusion, MSDC-0602K corrected glycemia and reduced insulinemia when given alone, or in combination with Lira. However, 0602K+Lira combination more significantly improved glucose tolerance and liver histology, suggesting that this combination treatment may be an effective therapeutic strategy for diabetes and NASH.
    MeSH term(s) Acetophenones/therapeutic use ; Animals ; Drug Therapy, Combination ; Female ; Hypoglycemic Agents/therapeutic use ; Insulin/metabolism ; Insulin Resistance ; Liraglutide/therapeutic use ; Male ; Mice ; Mice, Inbred C57BL ; Non-alcoholic Fatty Liver Disease/drug therapy ; Non-alcoholic Fatty Liver Disease/metabolism ; Thiazolidinediones/therapeutic use
    Chemical Substances Acetophenones ; Hypoglycemic Agents ; Insulin ; MSDC-0602 ; Thiazolidinediones ; Liraglutide (839I73S42A)
    Language English
    Publishing date 2021-05-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2021.100807
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.108: Show issues Location:
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