MicroRNA-29a is up-regulated in beta-cells by glucose and decreases glucose-stimulated insulin secretion
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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 tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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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