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  1. Article ; Online: Exercise and inactivity as modifiers of β cell function and type 2 diabetes risk.

    Hall, Liam G / Thyfault, John P / Johnson, James D

    Journal of applied physiology (Bethesda, Md. : 1985)

    2023  Volume 134, Issue 4, Page(s) 823–839

    Abstract: Exercise and regular physical activity are beneficial for the prevention and management of metabolic diseases such as obesity and type 2 diabetes, whereas exercise cessation, defined as deconditioning from regular exercise or physical activity that has ... ...

    Abstract Exercise and regular physical activity are beneficial for the prevention and management of metabolic diseases such as obesity and type 2 diabetes, whereas exercise cessation, defined as deconditioning from regular exercise or physical activity that has lasted for a period of months to years, can lead to metabolic derangements that drive disease. Adaptations to the insulin-secreting pancreatic β-cells are an important benefit of exercise, whereas less is known about how exercise cessation affects these cells. Our aim is to review the impact that exercise and exercise cessation have on β-cell function, with a focus on the evidence from studies examining glucose-stimulated insulin secretion (GSIS) using gold-standard techniques. Potential mechanisms by which the β-cell adapts to exercise, including exerkine and incretin signaling, autonomic nervous system signaling, and changes in insulin clearance, will also be explored. We will highlight areas for future research.
    MeSH term(s) Humans ; Diabetes Mellitus, Type 2/metabolism ; Insulin/metabolism ; Glucose/metabolism ; Insulin-Secreting Cells/metabolism ; Exercise/physiology
    Chemical Substances Insulin ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2023-02-09
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 219139-8
    ISSN 1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
    ISSN (online) 1522-1601
    ISSN 0021-8987 ; 0161-7567 ; 8750-7587
    DOI 10.1152/japplphysiol.00472.2022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Article ; Online: Amyloid beta 42 alters cardiac metabolism and impairs cardiac function in male mice with obesity.

    Hall, Liam G / Czeczor, Juliane K / Connor, Timothy / Botella, Javier / De Jong, Kirstie A / Renton, Mark C / Genders, Amanda J / Venardos, Kylie / Martin, Sheree D / Bond, Simon T / Aston-Mourney, Kathryn / Howlett, Kirsten F / Campbell, James A / Collier, Greg R / Walder, Ken R / McKenzie, Matthew / Ziemann, Mark / McGee, Sean L

    Nature communications

    2024  Volume 15, Issue 1, Page(s) 258

    Abstract: There are epidemiological associations between obesity and type 2 diabetes, cardiovascular disease and Alzheimer's disease. The role of amyloid beta 42 ( ... ...

    Abstract There are epidemiological associations between obesity and type 2 diabetes, cardiovascular disease and Alzheimer's disease. The role of amyloid beta 42 (Aβ
    MeSH term(s) Male ; Mice ; Animals ; Amyloid beta-Peptides ; Alzheimer Disease ; Diabetes Mellitus, Type 2/complications ; Antibodies, Neutralizing ; Obesity/complications ; Glucose ; Peptide Fragments
    Chemical Substances Amyloid beta-Peptides ; Antibodies, Neutralizing ; Glucose (IY9XDZ35W2) ; Peptide Fragments
    Language English
    Publishing date 2024-01-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-44520-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Loss of protein kinase D activity demonstrates redundancy in cardiac glucose metabolism and preserves cardiac function in obesity.

    De Jong, Kirstie A / Hall, Liam G / Renton, Mark C / Connor, Timothy / Martin, Sheree D / Kowalski, Greg M / Shaw, Christopher S / Bruce, Clinton R / Howlett, Kirsten F / McGee, Sean L

    Molecular metabolism

    2020  Volume 42, Page(s) 101105

    Abstract: Objective: Protein kinase D (PKD) signaling has been implicated in stress-induced cardiac remodeling and function as well as metabolic processes including contraction-mediated cardiac glucose uptake. PKD has recently emerged as a nutrient-sensing kinase ...

    Abstract Objective: Protein kinase D (PKD) signaling has been implicated in stress-induced cardiac remodeling and function as well as metabolic processes including contraction-mediated cardiac glucose uptake. PKD has recently emerged as a nutrient-sensing kinase that is activated in high-lipid environments, such as in obesity. However, the role of PKD signaling in cardiac glucose metabolism and cardiac function in both normal and obese conditions remains unknown.
    Methods: A cardiac-specific and inducible dominant negative (DN) PKD mouse model was developed. Echocardiography was used to assess cardiac function, while metabolic phenotyping was performed, including stable isotope metabolomics on cardiac tissue in mice fed either regular chow or a high-fat diet (43% calories from fat).
    Results: Cardiac PKD activity declined by ∼90% following DN PKD induction in adult mice. The mice had diminished basal cardiac glucose clearance, suggesting impaired contraction-mediated glucose uptake, but normal cardiac function. In obesity studies, systolic function indices were reduced in control mice, but not in cardiac DN PKD mice. Using targeted stable isotope metabolomic analyses, no differences in glucose flux through glycolysis or the TCA cycle were observed between groups.
    Conclusions: The data show that PKD contributes to cardiac dysfunction in obesity and highlight the redundancy in cardiac glucose metabolism that maintains cardiac glucose flux in vivo. The data suggest that impairments in contraction-mediated glucose uptake are unlikely to drive cardiac dysfunction in both normal and metabolic disease states.
    MeSH term(s) Animals ; Diet, High-Fat ; Female ; Gene Knock-In Techniques/methods ; Glucose/metabolism ; Heart/physiology ; Insulin/metabolism ; Insulin Resistance/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Myocardium/metabolism ; Myocytes, Cardiac/metabolism ; Obesity/metabolism ; Obesity/physiopathology ; Phosphorylation ; Protein Kinase C/genetics ; Protein Kinase C/metabolism ; Signal Transduction
    Chemical Substances Insulin ; protein kinase D (EC 2.7.10.-) ; Protein Kinase C (EC 2.7.11.13) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2020-10-21
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2708735-9
    ISSN 2212-8778 ; 2212-8778
    ISSN (online) 2212-8778
    ISSN 2212-8778
    DOI 10.1016/j.molmet.2020.101105
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: 1-Methyl-1

    Preston, Sarah / Garcia-Bustos, Jose / Hall, Liam G / Martin, Sheree D / Le, Thuy G / Kundu, Abhijit / Ghoshal, Atanu / Nguyen, Nghi H / Jiao, Yaqing / Ruan, Banfeng / Xue, Lian / Huang, Fei / Chang, Bill C H / McGee, Sean L / Wells, Timothy N C / Palmer, Michael J / Jabbar, Abdul / Gasser, Robin B / Baell, Jonathan B

    Journal of medicinal chemistry

    2020  Volume 64, Issue 1, Page(s) 840–844

    Abstract: A series of 1-methyl- ... ...

    Abstract A series of 1-methyl-1
    Language English
    Publishing date 2020-12-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218133-2
    ISSN 1520-4804 ; 0022-2623
    ISSN (online) 1520-4804
    ISSN 0022-2623
    DOI 10.1021/acs.jmedchem.0c01793
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MB 1: Show issues

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  5. Article ; Online: APP deficiency results in resistance to obesity but impairs glucose tolerance upon high fat feeding.

    Czeczor, Juliane K / Genders, Amanda J / Aston-Mourney, Kathryn / Connor, Timothy / Hall, Liam G / Hasebe, Kyoko / Ellis, Megan / De Jong, Kirstie A / Henstridge, Darren C / Meikle, Peter J / Febbraio, Mark A / Walder, Ken / McGee, Sean L

    The Journal of endocrinology

    2018  Volume 237, Issue 3, Page(s) 311–322

    Abstract: The amyloid precursor protein (APP) generates a number of peptides when processed through different cleavage mechanisms, including the amyloid beta peptide that is implicated in the development of Alzheimer's disease. It is well established that APP via ... ...

    Abstract The amyloid precursor protein (APP) generates a number of peptides when processed through different cleavage mechanisms, including the amyloid beta peptide that is implicated in the development of Alzheimer's disease. It is well established that APP via its cleaved peptides regulates aspects of neuronal metabolism. Emerging evidence suggests that amyloidogenic processing of APP can lead to altered systemic metabolism, similar to that observed in metabolic disease states. In the present study, we investigated the effect of APP deficiency on obesity-induced alterations in systemic metabolism. Compared with WT littermates, APP-deficient mice were resistant to diet-induced obesity, which was linked to higher energy expenditure and lipid oxidation throughout the dark phase and was associated with increased spontaneous physical activity. Consistent with this lean phenotype, APP-deficient mice fed a high-fat diet (HFD) had normal insulin tolerance. However, despite normal insulin action, these mice were glucose intolerant, similar to WT mice fed a HFD. This was associated with reduced plasma insulin in the early phase of the glucose tolerance test. Analysis of the pancreas showed that APP was required to maintain normal islet and β-cell mass under high fat feeding conditions. These studies show that, in addition to regulating aspects of neuronal metabolism, APP is an important regulator of whole body energy expenditure and glucose homeostasis under high fat feeding conditions.
    MeSH term(s) Amyloid beta-Peptides/genetics ; Animals ; Body Weight/genetics ; Carbohydrate Metabolism/genetics ; Diet, High-Fat/adverse effects ; Energy Metabolism/genetics ; Female ; Glucose/metabolism ; Glucose Intolerance/genetics ; Glucose Intolerance/metabolism ; Glucose Tolerance Test ; Insulin Resistance/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Obesity/genetics ; Obesity/metabolism
    Chemical Substances Amyloid beta-Peptides ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2018-04-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3028-4
    ISSN 1479-6805 ; 0022-0795
    ISSN (online) 1479-6805
    ISSN 0022-0795
    DOI 10.1530/JOE-18-0051
    Database MEDical Literature Analysis and Retrieval System OnLINE

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