KAT2B Is Required for Pancreatic Beta Cell Adaptation to Metabolic Stress by Controlling the Unfolded Protein Response.

Abstract:

:The endoplasmic reticulum (ER) unfolded protein response (UPR(er)) pathway plays an important role in helping pancreatic β cells to adapt their cellular responses to environmental cues and metabolic stress. Although altered UPR(er) gene expression appears in rodent and human type 2 diabetic (T2D) islets, the underlying molecular mechanisms remain unknown. We show here that germline and β cell-specific disruption of the lysine acetyltransferase 2B (Kat2b) gene in mice leads to impaired insulin secretion and glucose intolerance. Genome-wide analysis of Kat2b-regulated genes and functional assays reveal a critical role for Kat2b in maintaining UPR(er) gene expression and subsequent β cell function. Importantly, Kat2b expression is decreased in mouse and human diabetic β cells and correlates with UPR(er) gene expression in normal human islets. In conclusion, Kat2b is a crucial transcriptional regulator for adaptive β cell function during metabolic stress by controlling UPR(er) and represents a promising target for T2D prevention and treatment.

journal_name

Cell Rep

journal_title

Cell reports

authors

Rabhi N,Denechaud PD,Gromada X,Hannou SA,Zhang H,Rashid T,Salas E,Durand E,Sand O,Bonnefond A,Yengo L,Chavey C,Bonner C,Kerr-Conte J,Abderrahmani A,Auwerx J,Fajas L,Froguel P,Annicotte JS

doi

10.1016/j.celrep.2016.03.079

subject

Has Abstract

pub_date

2016-05-03 00:00:00

pages

1051-1061

issue

5

issn

2211-1247

pii

S2211-1247(16)30368-0

journal_volume

15

pub_type

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