METTL3 is required for maintaining β-cell function

Xinzhi Li; Yuze Jiang; Xu Sun; Yongsen Wu; Zheng Chen

doi:10.1016/j.metabol.2021.154702

METTL3 is required for maintaining β-cell function

Xinzhi Li
, Yuze Jiang
, Xu Sun
, Yongsen Wu
, Zheng Chen^*

^*Corresponding author for this work

School of Life Science and Technology, Harbin Institute of Technology

Research output: Contribution to journal › Article › peer-review

76 Scopus citations

Abstract

N6-methyladenosine (m⁶A) mRNA methylation has been shown to regulate obesity and type 2 diabetes. However, whether METTL3, the key methyltransferase for m⁶A mRNA methylation, regulates β-cell failure in diabetes has not been fully explored. Here, we show that METTL3 is downregulated under the inflammatory and oxidative stress conditions, and islet β-cell-specific deletion of Mettl3 induces β-cell failure and hyperglycemia, which is likely due to decreased m⁶A modification and reduced expression of insulin secretion-related genes. Overall, METTL3 might be a potential drug target for the treatment of β-cell failure in diabetes.

Original language	English
Article number	154702
Journal	Metabolism: Clinical and Experimental
Volume	116
DOIs	https://doi.org/10.1016/j.metabol.2021.154702
State	Published - Mar 2021
Externally published	Yes

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Cell death
Hyperglycemia
Insulin secretion
Islet β cells
METTL3
mA

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10.1016/j.metabol.2021.154702

Cite this

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title = "METTL3 is required for maintaining β-cell function",

abstract = "N6-methyladenosine (m6A) mRNA methylation has been shown to regulate obesity and type 2 diabetes. However, whether METTL3, the key methyltransferase for m6A mRNA methylation, regulates β-cell failure in diabetes has not been fully explored. Here, we show that METTL3 is downregulated under the inflammatory and oxidative stress conditions, and islet β-cell-specific deletion of Mettl3 induces β-cell failure and hyperglycemia, which is likely due to decreased m6A modification and reduced expression of insulin secretion-related genes. Overall, METTL3 might be a potential drug target for the treatment of β-cell failure in diabetes.",

keywords = "Cell death, Hyperglycemia, Insulin secretion, Islet β cells, METTL3, mA",

author = "Xinzhi Li and Yuze Jiang and Xu Sun and Yongsen Wu and Zheng Chen",

note = "Publisher Copyright: {\textcopyright} 2021 Elsevier Inc.",

year = "2021",

month = mar,

doi = "10.1016/j.metabol.2021.154702",

language = "英语",

volume = "116",

journal = "Metabolism: Clinical and Experimental",

issn = "0026-0495",

publisher = "W.B. Saunders",

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TY - JOUR

T1 - METTL3 is required for maintaining β-cell function

AU - Li, Xinzhi

AU - Jiang, Yuze

AU - Sun, Xu

AU - Wu, Yongsen

AU - Chen, Zheng

PY - 2021/3

Y1 - 2021/3

N2 - N6-methyladenosine (m6A) mRNA methylation has been shown to regulate obesity and type 2 diabetes. However, whether METTL3, the key methyltransferase for m6A mRNA methylation, regulates β-cell failure in diabetes has not been fully explored. Here, we show that METTL3 is downregulated under the inflammatory and oxidative stress conditions, and islet β-cell-specific deletion of Mettl3 induces β-cell failure and hyperglycemia, which is likely due to decreased m6A modification and reduced expression of insulin secretion-related genes. Overall, METTL3 might be a potential drug target for the treatment of β-cell failure in diabetes.

AB - N6-methyladenosine (m6A) mRNA methylation has been shown to regulate obesity and type 2 diabetes. However, whether METTL3, the key methyltransferase for m6A mRNA methylation, regulates β-cell failure in diabetes has not been fully explored. Here, we show that METTL3 is downregulated under the inflammatory and oxidative stress conditions, and islet β-cell-specific deletion of Mettl3 induces β-cell failure and hyperglycemia, which is likely due to decreased m6A modification and reduced expression of insulin secretion-related genes. Overall, METTL3 might be a potential drug target for the treatment of β-cell failure in diabetes.

KW - Cell death

KW - Hyperglycemia

KW - Insulin secretion

KW - Islet β cells

KW - METTL3

KW - mA

UR - https://www.scopus.com/pages/publications/85099296124

U2 - 10.1016/j.metabol.2021.154702

DO - 10.1016/j.metabol.2021.154702

M3 - 文章

C2 - 33417895

AN - SCOPUS:85099296124

SN - 0026-0495

VL - 116

JO - Metabolism: Clinical and Experimental

JF - Metabolism: Clinical and Experimental

M1 - 154702

ER -

METTL3 is required for maintaining β-cell function

Abstract

UN SDGs

Keywords

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