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  1. 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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  2. Article: Markers of increased cardiovascular risk: are we measuring the most appropriate parameters?

    Hawkins, Meredith A

    Obesity research

    2004  Volume 12 Suppl 2, Page(s) 107S–14S

    Abstract: The vital task of evaluating cardiovascular disease risk in individual patients is challenging in light of the ever-growing list of risk factors. Some of the traditional measures of cardiovascular risk, such as blood lipid levels, have been further ... ...

    Abstract The vital task of evaluating cardiovascular disease risk in individual patients is challenging in light of the ever-growing list of risk factors. Some of the traditional measures of cardiovascular risk, such as blood lipid levels, have been further refined to provide better risk assessments. Certain specific parameters, such as lipoprotein buoyancy, seem to be better predictors of cardiovascular disease than total lipoprotein levels. Furthermore, as the contribution of systemic inflammation to the pathogenesis of atherosclerosis is increasingly recognized, several inflammatory markers have become associated with disease risk. Consequently, many studies have attempted to determine the individual merits of these factors in predicting cardiovascular risk.
    MeSH term(s) Biomarkers/analysis ; Blood Glucose ; C-Reactive Protein ; Cardiovascular Diseases ; Chemical Phenomena ; Chemistry, Physical ; Diabetes Mellitus ; Glycated Hemoglobin A ; Humans ; Insulin Resistance ; Lipids/blood ; Lipoproteins, LDL/blood ; Metabolic Syndrome ; Obesity ; Risk Factors ; Viscera
    Chemical Substances Biomarkers ; Blood Glucose ; Glycated Hemoglobin A ; Lipids ; Lipoproteins, LDL ; C-Reactive Protein (9007-41-4)
    Language English
    Publishing date 2004-11
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1201744-9
    ISSN 1550-8528 ; 1071-7323
    ISSN (online) 1550-8528
    ISSN 1071-7323
    DOI 10.1038/oby.2004.275
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4061: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
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  3. Article ; Online: β-cell failure in type 2 diabetes: postulated mechanisms and prospects for prevention and treatment.

    Halban, Philippe A / Polonsky, Kenneth S / Bowden, Donald W / Hawkins, Meredith A / Ling, Charlotte / Mather, Kieren J / Powers, Alvin C / Rhodes, Christopher J / Sussel, Lori / Weir, Gordon C

    Diabetes care

    2014  Volume 37, Issue 6, Page(s) 1751–1758

    Abstract: Objective: This article examines the foundation of β-cell failure in type 2 diabetes (T2D) and suggests areas for future research on the underlying mechanisms that may lead to improved prevention and treatment.: Research design and methods: A group ... ...

    Abstract Objective: This article examines the foundation of β-cell failure in type 2 diabetes (T2D) and suggests areas for future research on the underlying mechanisms that may lead to improved prevention and treatment.
    Research design and methods: A group of experts participated in a conference on 14-16 October 2013 cosponsored by the Endocrine Society and the American Diabetes Association. A writing group prepared this summary and recommendations.
    Results: The writing group based this article on conference presentations, discussion, and debate. Topics covered include genetic predisposition, foundations of β-cell failure, natural history of β-cell failure, and impact of therapeutic interventions.
    Conclusions: β-Cell failure is central to the development and progression of T2D. It antedates and predicts diabetes onset and progression, is in part genetically determined, and often can be identified with accuracy even though current tests are cumbersome and not well standardized. Multiple pathways underlie decreased β-cell function and mass, some of which may be shared and may also be a consequence of processes that initially caused dysfunction. Goals for future research include to (1) impact the natural history of β-cell failure; (2) identify and characterize genetic loci for T2D; (3) target β-cell signaling, metabolic, and genetic pathways to improve function/mass; (4) develop alternative sources of β-cells for cell-based therapy; (5) focus on metabolic environment to provide indirect benefit to β-cells; (6) improve understanding of the physiology of responses to bypass surgery; and (7) identify circulating factors and neuronal circuits underlying the axis of communication between the brain and β-cells.
    MeSH term(s) Congresses as Topic ; Diabetes Mellitus, Type 2/physiopathology ; Diabetes Mellitus, Type 2/prevention & control ; Expert Testimony ; Genetic Predisposition to Disease ; Humans ; Insulin-Secreting Cells/pathology ; Insulin-Secreting Cells/physiology ; Signal Transduction
    Language English
    Publishing date 2014-05-08
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 441231-x
    ISSN 1935-5548 ; 0149-5992
    ISSN (online) 1935-5548
    ISSN 0149-5992
    DOI 10.2337/dc14-0396
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1434: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
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    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 365: Show issues

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  4. Article ; Online: β-cell failure in type 2 diabetes: postulated mechanisms and prospects for prevention and treatment.

    Halban, Philippe A / Polonsky, Kenneth S / Bowden, Donald W / Hawkins, Meredith A / Ling, Charlotte / Mather, Kieren J / Powers, Alvin C / Rhodes, Christopher J / Sussel, Lori / Weir, Gordon C

    The Journal of clinical endocrinology and metabolism

    2014  Volume 99, Issue 6, Page(s) 1983–1992

    Abstract: Objective: This article examines the foundation of β-cell failure in type 2 diabetes (T2D) and suggests areas for future research on the underlying mechanisms that may lead to improved prevention and treatment.: Research design and methods: A group ... ...

    Abstract Objective: This article examines the foundation of β-cell failure in type 2 diabetes (T2D) and suggests areas for future research on the underlying mechanisms that may lead to improved prevention and treatment.
    Research design and methods: A group of experts participated in a conference on 14-16 October 2013 cosponsored by the Endocrine Society and the American Diabetes Association. A writing group prepared this summary and recommendations.
    Results: The writing group based this article on conference presentations, discussion, and debate. Topics covered include genetic predisposition, foundations of β-cell failure, natural history of β-cell failure, and impact of therapeutic interventions.
    Conclusions: β-Cell failure is central to the development and progression of T2D. It antedates and predicts diabetes onset and progression, is in part genetically determined, and often can be identified with accuracy even though current tests are cumbersome and not well standardized. Multiple pathways underlie decreased β-cell function and mass, some of which may be shared and may also be a consequence of processes that initially caused dysfunction. Goals for future research include to 1) impact the natural history of β-cell failure; 2) identify and characterize genetic loci for T2D; 3) target β-cell signaling, metabolic, and genetic pathways to improve function/mass; 4) develop alternative sources of β-cells for cell-based therapy; 5) focus on metabolic environment to provide indirect benefit to β-cells; 6) improve understanding of the physiology of responses to bypass surgery; and 7) identify circulating factors and neuronal circuits underlying the axis of communication between the brain and β-cells.
    MeSH term(s) Cell Death ; Cell Dedifferentiation ; Diabetes Mellitus, Type 2/etiology ; Diabetes Mellitus, Type 2/physiopathology ; Diabetes Mellitus, Type 2/therapy ; Endoplasmic Reticulum Stress ; Epigenesis, Genetic ; Humans ; Inflammation/complications ; Inflammation/metabolism ; Insulin-Secreting Cells/pathology ; Insulin-Secreting Cells/physiology ; Oxidative Stress ; Plaque, Amyloid/metabolism ; Preventive Medicine/trends ; Signal Transduction/genetics
    Language English
    Publishing date 2014-04-08
    Publishing country United States
    Document type Consensus Development Conference ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3029-6
    ISSN 1945-7197 ; 0021-972X
    ISSN (online) 1945-7197
    ISSN 0021-972X
    DOI 10.1210/jc.2014-1425
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uh III Zs.134: Show issues Location:
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