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  1. Artikel ; Online: MafA Regulation in β-Cells: From Transcriptional to Post-Translational Mechanisms.

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

    Biomolecules

    2022  Band 12, Heft 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-Begriff(e) 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
    Chemische Substanzen Insulin ; Maf Transcription Factors, Large
    Sprache Englisch
    Erscheinungsdatum 2022-03-31
    Erscheinungsland Switzerland
    Dokumenttyp 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
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: TGR5 Signaling in Hepatic Metabolic Health.

    Holter, Marlena M / Chirikjian, Margot K / Govani, Viraj N / Cummings, Bethany P

    Nutrients

    2020  Band 12, Heft 9

    Abstract: TGR5 is a G protein-coupled bile acid receptor that is increasingly recognized as a key regulator of glucose homeostasis. While the role of TGR5 signaling in immune cells, adipocytes and enteroendocrine L cells in metabolic regulation has been well ... ...

    Abstract TGR5 is a G protein-coupled bile acid receptor that is increasingly recognized as a key regulator of glucose homeostasis. While the role of TGR5 signaling in immune cells, adipocytes and enteroendocrine L cells in metabolic regulation has been well described and extensively reviewed, the impact of TGR5-mediated effects on hepatic physiology and pathophysiology in metabolic regulation has received less attention. Recent studies suggest that TGR5 signaling contributes to improvements in hepatic insulin signaling and decreased hepatic inflammation, as well as metabolically beneficial improvements in bile acid profile. Additionally, TGR5 signaling has been associated with reduced hepatic steatosis and liver fibrosis, and improved liver function. Despite the beneficial effects of TGR5 signaling on metabolic health, TGR5-mediated gallstone formation and gallbladder filling complicate therapeutic targeting of TGR5 signaling. To this end, there is a growing need to identify cell type-specific effects of hepatic TGR5 signaling to begin to identify and target the downstream effectors of TGR5 signaling. Herein, we describe and integrate recent advances in our understanding of the impact of TGR5 signaling on liver physiology and how its effects on the liver integrate more broadly with whole body glucose regulation.
    Mesh-Begriff(e) Humans ; Liver/metabolism ; Liver/physiology ; Receptors, G-Protein-Coupled/metabolism ; Receptors, G-Protein-Coupled/physiology ; Signal Transduction/physiology
    Chemische Substanzen GPBAR1 protein, human ; Receptors, G-Protein-Coupled
    Sprache Englisch
    Erscheinungsdatum 2020-08-26
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2518386-2
    ISSN 2072-6643 ; 2072-6643
    ISSN (online) 2072-6643
    ISSN 2072-6643
    DOI 10.3390/nu12092598
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: TGR5 Signaling in Hepatic Metabolic Health

    Holter, Marlena M / Chirikjian, Margot K / Govani, Viraj N / Cummings, Bethany P

    Nutrients. 2020 Aug. 26, v. 12, no. 9

    2020  

    Abstract: TGR5 is a G protein-coupled bile acid receptor that is increasingly recognized as a key regulator of glucose homeostasis. While the role of TGR5 signaling in immune cells, adipocytes and enteroendocrine L cells in metabolic regulation has been well ... ...

    Abstract TGR5 is a G protein-coupled bile acid receptor that is increasingly recognized as a key regulator of glucose homeostasis. While the role of TGR5 signaling in immune cells, adipocytes and enteroendocrine L cells in metabolic regulation has been well described and extensively reviewed, the impact of TGR5-mediated effects on hepatic physiology and pathophysiology in metabolic regulation has received less attention. Recent studies suggest that TGR5 signaling contributes to improvements in hepatic insulin signaling and decreased hepatic inflammation, as well as metabolically beneficial improvements in bile acid profile. Additionally, TGR5 signaling has been associated with reduced hepatic steatosis and liver fibrosis, and improved liver function. Despite the beneficial effects of TGR5 signaling on metabolic health, TGR5-mediated gallstone formation and gallbladder filling complicate therapeutic targeting of TGR5 signaling. To this end, there is a growing need to identify cell type-specific effects of hepatic TGR5 signaling to begin to identify and target the downstream effectors of TGR5 signaling. Herein, we describe and integrate recent advances in our understanding of the impact of TGR5 signaling on liver physiology and how its effects on the liver integrate more broadly with whole body glucose regulation.
    Schlagwörter adipocytes ; bile acids ; cholelithiasis ; fatty liver ; gall bladder ; glucose ; homeostasis ; inflammation ; insulin ; liver ; liver cirrhosis ; liver function ; pathophysiology ; therapeutics
    Sprache Englisch
    Erscheinungsverlauf 2020-0826
    Erscheinungsort Multidisciplinary Digital Publishing Institute
    Dokumenttyp Artikel
    Anmerkung NAL-light
    ZDB-ID 2518386-2
    ISSN 2072-6643
    ISSN 2072-6643
    DOI 10.3390/nu12092598
    Datenquelle NAL Katalog (AGRICOLA)

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  4. Artikel ; Online: Compound 18 Improves Glucose Tolerance in a Hepatocyte TGR5-dependent Manner in Mice.

    Holter, Marlena M / Chirikjian, Margot K / Briere, Daniel A / Maida, Adriano / Sloop, Kyle W / Schoonjans, Kristina / Cummings, Bethany P

    Nutrients

    2020  Band 12, Heft 7

    Abstract: The bile acid receptor, TGR5, is a key regulator of glucose homeostasis, but the mechanisms by which TGR5 signaling improves glucose regulation are incompletely defined. In particular, TGR5 has an increasingly appreciated role in liver physiology and ... ...

    Abstract The bile acid receptor, TGR5, is a key regulator of glucose homeostasis, but the mechanisms by which TGR5 signaling improves glucose regulation are incompletely defined. In particular, TGR5 has an increasingly appreciated role in liver physiology and pathobiology; however, whether TGR5 signaling within the liver contributes to its glucoregulatory effects is unknown. Therefore, we investigated the role of hepatocyte TGR5 signaling on glucose regulation using a hepatocyte-specific TGR5 knockout mouse model. Hepatocyte-specific
    Mesh-Begriff(e) Adiposity/drug effects ; Animals ; Blood Glucose/metabolism ; Body Weight ; Diet, High-Fat ; Female ; Glucagon-Like Peptide 1/metabolism ; Glucose Tolerance Test ; Hepatocytes/drug effects ; Hepatocytes/metabolism ; Homeostasis ; Insulin Resistance ; Liver/drug effects ; Liver/metabolism ; Male ; Mice ; Mice, Knockout ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction ; Triiodobenzoic Acids/pharmacology
    Chemische Substanzen Blood Glucose ; Gpbar1 protein, mouse ; Receptors, G-Protein-Coupled ; Triiodobenzoic Acids ; compound 18 (31112-66-0) ; Glucagon-Like Peptide 1 (89750-14-1)
    Sprache Englisch
    Erscheinungsdatum 2020-07-17
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2518386-2
    ISSN 2072-6643 ; 2072-6643
    ISSN (online) 2072-6643
    ISSN 2072-6643
    DOI 10.3390/nu12072124
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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