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

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Standard

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

I: Biochemical and Biophysical Research Communications, Bind 426, Nr. 2, 21.09.2012, s. 266-72.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Bagge, A, Clausen, TR, Larsen, S, Ladefoged, M, Rosenstierne, MW, Larsen, L, Vang, O, Nielsen, JH & Dalgaard, LT 2012, 'MicroRNA-29a is up-regulated in beta-cells by glucose and decreases glucose-stimulated insulin secretion', Biochemical and Biophysical Research Communications, bind 426, nr. 2, s. 266-72. https://doi.org/10.1016/j.bbrc.2012.08.082

APA

Bagge, A., Clausen, T. R., Larsen, S., Ladefoged, M., Rosenstierne, M. W., Larsen, L., ... Dalgaard, L. T. (2012). MicroRNA-29a is up-regulated in beta-cells by glucose and decreases glucose-stimulated insulin secretion. Biochemical and Biophysical Research Communications, 426(2), 266-72. https://doi.org/10.1016/j.bbrc.2012.08.082

Vancouver

Bagge A, Clausen TR, Larsen S, Ladefoged M, Rosenstierne MW, Larsen L o.a. MicroRNA-29a is up-regulated in beta-cells by glucose and decreases glucose-stimulated insulin secretion. Biochemical and Biophysical Research Communications. 2012 sep 21;426(2):266-72. https://doi.org/10.1016/j.bbrc.2012.08.082

Author

Bagge, Annika ; Clausen, Trine R ; Larsen, Sylvester ; Ladefoged, Mette ; Rosenstierne, Maiken W ; Larsen, Louise ; Vang, Ole ; Nielsen, Jens Høiriis ; Dalgaard, Louise T. / 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. 266-72.

Bibtex

@article{b914a2d151054d84b167e22a8b1b8743,
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 = "Animals, Cell Line, Cell Proliferation, Cell Size, Glucose, Glucose Intolerance, Humans, Insulin, Insulin-Secreting Cells, MicroRNAs, Rats, Up-Regulation",
author = "Annika Bagge and Clausen, {Trine R} and Sylvester Larsen and Mette Ladefoged and Rosenstierne, {Maiken W} and Louise Larsen and Ole Vang and Nielsen, {Jens H{\o}iriis} and Dalgaard, {Louise T}",
note = "Copyright {\circledC} 2012 Elsevier Inc. All rights reserved.",
year = "2012",
month = "9",
day = "21",
doi = "10.1016/j.bbrc.2012.08.082",
language = "English",
volume = "426",
pages = "266--72",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Elsevier",
number = "2",

}

RIS

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 R

AU - Larsen, Sylvester

AU - Ladefoged, Mette

AU - Rosenstierne, Maiken W

AU - Larsen, Louise

AU - Vang, Ole

AU - Nielsen, Jens Høiriis

AU - Dalgaard, Louise T

N1 - Copyright © 2012 Elsevier Inc. All rights reserved.

PY - 2012/9/21

Y1 - 2012/9/21

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 - Animals

KW - Cell Line

KW - Cell Proliferation

KW - Cell Size

KW - Glucose

KW - Glucose Intolerance

KW - Humans

KW - Insulin

KW - Insulin-Secreting Cells

KW - MicroRNAs

KW - Rats

KW - Up-Regulation

U2 - 10.1016/j.bbrc.2012.08.082

DO - 10.1016/j.bbrc.2012.08.082

M3 - Journal article

C2 - 22940552

VL - 426

SP - 266

EP - 272

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 2

ER -

ID: 47972027