PMID- 29191656
OWN - NLM
STAT- MEDLINE
DCOM- 20171228
LR  - 20180105
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 495
IP  - 1
DP  - 2018 Jan 1
TI  - Overexpression of microRNA-26a protects against deficient beta-cell function via 
      targeting phosphatase with tensin homology in mouse models of type 2 diabetes.
PG  - 1312-1316
LID - S0006-291X(17)32348-3 [pii]
LID - 10.1016/j.bbrc.2017.11.170 [doi]
AB  - The prevalence of type 2 diabetes mellitus (T2DM) increased rapidly in the world. 
      The development of beta-cell dysfunction is the quintessential defects in T2DM 
      patients However, the pathogenesis of beta-cell dysfunction is still unclear. 
      MicroRNAs are short non-coding RNAs and has been reported to be involved in 
      pathogenesis of beta-cell dysfunction and T2DM. Here, we investigated the mechanisms 
      by which miR-26a regulate beta-cell function and insulin signaling pathway in high 
      fat diet (HFD) fed and db/db T2DM mice model. The expression of miR-26a was 
      down-regulated dramatically in the serum and islets of both HFD and db/db mice 
      model. miR-26a overexpression protected against HFD-induced diabetes and 
      maintained prolonged normoglycemic time in HFD fed mice. Overexpression of 
      miR-26a improved beta-cell dysfunction in T2DM mice. Further, we identified that 
      PTEN is a direct target gene of miR-26a. Overexpression of miR-26a significantly 
      inhibited the luciferase activity of hPTEN 3'-UTR, while the effect of miR-26a 
      disappeared when the miR-26a potential binding site within the PTEN 3'-UTR was 
      mutated. Overexpression of miR-26a reduced both the mRNA and protein levels of 
      PTEN in vitro and in vivo. We also found that miR-26a overexpression increased 
      the expression of p-Akt and p-FoxO-1, while the effect of miR-26a was blocked by 
      PTEN overexpression. In conclusion, our data indicated that miR-26a potentially 
      contributes to the beta-cell dysfunction in T2DM, and miR-26a may be a new 
      therapeutic strategy against T2DM.
CI  - Copyright (c) 2017 Elsevier Inc. All rights reserved.
FAU - Song, Yingli
AU  - Song Y
AD  - Department of Physiology, College of Basic Medical Science, Harbin Medical 
      University, Harbin, China.
FAU - Jin, Di
AU  - Jin D
AD  - Department of Geriatrics, The Second Affiliated Hospital of Harbin Medical 
      University, Harbin, China.
FAU - Jiang, Xiaoshu
AU  - Jiang X
AD  - Department of Physiology, College of Basic Medical Science, Harbin Medical 
      University, Harbin, China.
FAU - Lv, Chunmei
AU  - Lv C
AD  - Department of Physiology, College of Basic Medical Science, Harbin Medical 
      University, Harbin, China.
FAU - Zhu, Hui
AU  - Zhu H
AD  - Department of Physiology, College of Basic Medical Science, Harbin Medical 
      University, Harbin, China. Electronic address: huizhu123@126.com.
LA  - eng
PT  - Journal Article
DEP - 20171202
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Insulin)
RN  - 0 (MicroRNAs)
RN  - 0 (Mirn26 microRNA, mouse)
RN  - EC 3.1.3.67 (PTEN Phosphohydrolase)
RN  - EC 3.1.3.67 (Pten protein, mouse)
SB  - IM
MH  - Animals
MH  - Diabetes Mellitus, Type 2/*metabolism/pathology
MH  - Insulin/*metabolism
MH  - Insulin-Secreting Cells/*metabolism/*pathology
MH  - Male
MH  - Mice
MH  - MicroRNAs/*metabolism
MH  - PTEN Phosphohydrolase/*metabolism
MH  - Up-Regulation
OTO - NOTNLM
OT  - MiR-26a
OT  - PTEN
OT  - T2DM
OT  - beta-cell function
EDAT- 2017/12/02 06:00
MHDA- 2017/12/29 06:00
CRDT- 2017/12/02 06:00
PHST- 2017/11/21 00:00 [received]
PHST- 2017/11/26 00:00 [accepted]
PHST- 2017/12/02 06:00 [pubmed]
PHST- 2017/12/29 06:00 [medline]
PHST- 2017/12/02 06:00 [entrez]
AID - S0006-291X(17)32348-3 [pii]
AID - 10.1016/j.bbrc.2017.11.170 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2018 Jan 1;495(1):1312-1316. doi: 
      10.1016/j.bbrc.2017.11.170. Epub 2017 Dec 2.