MicroRNA-29a is up-regulated in beta-cells by glucose and decreases glucose-stimulated insulin secretion

Annika Bagge, Trine Ryberg Clausen, Mette Ladefoged, Maiken Worsøe Rosenstierne, Larsen Louise, Ole Vang, Jens Høiriis Nielsen, Louise Torp Dalgaard, Sylvester Larsen

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

    Resumé

    Chronically elevated levels of glucose impair pancreatic beta-cell function while inducing beta-cell proliferation. MicroRNA-29a (miR-29a) levels are increased in several tissues in diabetic animals and mediate decreased insulin-stimulated glucose-transport of adipocytes. The aim was to investigate the impact of glucose on miR-29a levels in INS-1E beta-cells and in human islets of Langerhans and furthermore to evaluate the impact of miR-29a on beta-cell function and proliferation. Increased glucose levels up-regulated miR-29a in beta-cells and human and rat islets of Langerhans. Glucose-stimulated insulin-secretion (GSIS) of INS-1E beta-cells was decreased by forced expression of miR-29a, while depletion of endogenous miR-29a improved GSIS. Over-expression of miR-29a increased INS-1E proliferation. Thus, miR-29a up-regulation is involved in glucose-induced proliferation of beta-cells. Furthermore, as depletion of miR-29a improves beta-cell function, miR-29a is a mediator of glucose-induced beta-cell dysfunction. Glucose-induced up-regulation of miR-29a in beta-cells could be implicated in progression from impaired glucose tolerance to type 2 diabetes.
    OriginalsprogEngelsk
    TidsskriftBiochemical and Biophysical Research Communications
    Vol/bind426
    Udgave nummer2
    Sider (fra-til)266-272
    ISSN0006-291X
    DOI
    StatusUdgivet - 2012

    Citer dette

    Bagge, Annika ; Clausen, Trine Ryberg ; Ladefoged, Mette ; Rosenstierne, Maiken Worsøe ; Louise, Larsen ; Vang, Ole ; Nielsen, Jens Høiriis ; Dalgaard, Louise Torp ; Larsen, Sylvester. / MicroRNA-29a is up-regulated in beta-cells by glucose and decreases glucose-stimulated insulin secretion. I: Biochemical and Biophysical Research Communications. 2012 ; Bind 426, Nr. 2. s. 266-272.
    @article{596ea7dcb9164cba8f575d938c0d76ce,
    title = "MicroRNA-29a is up-regulated in beta-cells by glucose and decreases glucose-stimulated insulin secretion",
    abstract = "Chronically elevated levels of glucose impair pancreatic beta-cell function while inducing beta-cell proliferation. MicroRNA-29a (miR-29a) levels are increased in several tissues in diabetic animals and mediate decreased insulin-stimulated glucose-transport of adipocytes. The aim was to investigate the impact of glucose on miR-29a levels in INS-1E beta-cells and in human islets of Langerhans and furthermore to evaluate the impact of miR-29a on beta-cell function and proliferation. Increased glucose levels up-regulated miR-29a in beta-cells and human and rat islets of Langerhans. Glucose-stimulated insulin-secretion (GSIS) of INS-1E beta-cells was decreased by forced expression of miR-29a, while depletion of endogenous miR-29a improved GSIS. Over-expression of miR-29a increased INS-1E proliferation. Thus, miR-29a up-regulation is involved in glucose-induced proliferation of beta-cells. Furthermore, as depletion of miR-29a improves beta-cell function, miR-29a is a mediator of glucose-induced beta-cell dysfunction. Glucose-induced up-regulation of miR-29a in beta-cells could be implicated in progression from impaired glucose tolerance to type 2 diabetes.",
    keywords = "MicroRNA, Beta-cell, Islets of Langerhans, MicroRNA-29a, Glucose toxicity, Beta-cell dysfunction",
    author = "Annika Bagge and Clausen, {Trine Ryberg} and Mette Ladefoged and Rosenstierne, {Maiken Wors{\o}e} and Larsen Louise and Ole Vang and Nielsen, {Jens H{\o}iriis} and Dalgaard, {Louise Torp} and Sylvester Larsen",
    year = "2012",
    doi = "10.1016/j.bbrc.2012.08.082",
    language = "English",
    volume = "426",
    pages = "266--272",
    journal = "Biochemical and Biophysical Research Communications",
    issn = "0006-291X",
    publisher = "Elsevier Inc.",
    number = "2",

    }

    MicroRNA-29a is up-regulated in beta-cells by glucose and decreases glucose-stimulated insulin secretion. / Bagge, Annika; Clausen, Trine Ryberg; Ladefoged, Mette; Rosenstierne, Maiken Worsøe; Louise, Larsen ; Vang, Ole; Nielsen, Jens Høiriis ; Dalgaard, Louise Torp; Larsen, Sylvester.

    I: Biochemical and Biophysical Research Communications, Bind 426, Nr. 2, 2012, s. 266-272.

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

    TY - JOUR

    T1 - MicroRNA-29a is up-regulated in beta-cells by glucose and decreases glucose-stimulated insulin secretion

    AU - Bagge, Annika

    AU - Clausen, Trine Ryberg

    AU - Ladefoged, Mette

    AU - Rosenstierne, Maiken Worsøe

    AU - Louise, Larsen

    AU - Vang, Ole

    AU - Nielsen, Jens Høiriis

    AU - Dalgaard, Louise Torp

    AU - Larsen, Sylvester

    PY - 2012

    Y1 - 2012

    N2 - Chronically elevated levels of glucose impair pancreatic beta-cell function while inducing beta-cell proliferation. MicroRNA-29a (miR-29a) levels are increased in several tissues in diabetic animals and mediate decreased insulin-stimulated glucose-transport of adipocytes. The aim was to investigate the impact of glucose on miR-29a levels in INS-1E beta-cells and in human islets of Langerhans and furthermore to evaluate the impact of miR-29a on beta-cell function and proliferation. Increased glucose levels up-regulated miR-29a in beta-cells and human and rat islets of Langerhans. Glucose-stimulated insulin-secretion (GSIS) of INS-1E beta-cells was decreased by forced expression of miR-29a, while depletion of endogenous miR-29a improved GSIS. Over-expression of miR-29a increased INS-1E proliferation. Thus, miR-29a up-regulation is involved in glucose-induced proliferation of beta-cells. Furthermore, as depletion of miR-29a improves beta-cell function, miR-29a is a mediator of glucose-induced beta-cell dysfunction. Glucose-induced up-regulation of miR-29a in beta-cells could be implicated in progression from impaired glucose tolerance to type 2 diabetes.

    AB - Chronically elevated levels of glucose impair pancreatic beta-cell function while inducing beta-cell proliferation. MicroRNA-29a (miR-29a) levels are increased in several tissues in diabetic animals and mediate decreased insulin-stimulated glucose-transport of adipocytes. The aim was to investigate the impact of glucose on miR-29a levels in INS-1E beta-cells and in human islets of Langerhans and furthermore to evaluate the impact of miR-29a on beta-cell function and proliferation. Increased glucose levels up-regulated miR-29a in beta-cells and human and rat islets of Langerhans. Glucose-stimulated insulin-secretion (GSIS) of INS-1E beta-cells was decreased by forced expression of miR-29a, while depletion of endogenous miR-29a improved GSIS. Over-expression of miR-29a increased INS-1E proliferation. Thus, miR-29a up-regulation is involved in glucose-induced proliferation of beta-cells. Furthermore, as depletion of miR-29a improves beta-cell function, miR-29a is a mediator of glucose-induced beta-cell dysfunction. Glucose-induced up-regulation of miR-29a in beta-cells could be implicated in progression from impaired glucose tolerance to type 2 diabetes.

    KW - MicroRNA

    KW - Beta-cell

    KW - Islets of Langerhans

    KW - MicroRNA-29a

    KW - Glucose toxicity

    KW - Beta-cell dysfunction

    U2 - 10.1016/j.bbrc.2012.08.082

    DO - 10.1016/j.bbrc.2012.08.082

    M3 - Journal article

    VL - 426

    SP - 266

    EP - 272

    JO - Biochemical and Biophysical Research Communications

    JF - Biochemical and Biophysical Research Communications

    SN - 0006-291X

    IS - 2

    ER -