O-linked N-acetylglucosamine transferase (OGT) regulates pancreatic α-cell function in mice.
Acylation
/ drug effects
Animals
Blood Glucose
/ metabolism
Fasting
/ metabolism
Female
Founder Effect
Glucagon
/ biosynthesis
Glucagon-Secreting Cells
/ drug effects
Gluconeogenesis
/ drug effects
Glucose Tolerance Test
Hepatocyte Nuclear Factor 3-beta
/ genetics
Insulin Resistance
Integrases
/ genetics
Male
Mice
Mice, Knockout
N-Acetylglucosaminyltransferases
/ deficiency
Obesity
/ enzymology
Pyruvic Acid
/ metabolism
O-GlcNAcylation
O-linked N-acetylglucosamine (GlcNAc) transferase
apoptosis
carboxypeptidase E
diabetes
glucagon
pancreatic alpha cell
proglucagon
Journal
The Journal of biological chemistry
ISSN: 1083-351X
Titre abrégé: J Biol Chem
Pays: United States
ID NLM: 2985121R
Informations de publication
Date de publication:
Historique:
received:
03
08
2020
revised:
05
01
2021
accepted:
12
01
2021
pubmed:
19
1
2021
medline:
1
9
2021
entrez:
18
1
2021
Statut:
ppublish
Résumé
The nutrient sensor O-GlcNAc transferase (OGT) catalyzes posttranslational addition of O-GlcNAc onto target proteins, influencing signaling pathways in response to cellular nutrient levels. OGT is highly expressed in pancreatic glucagon-secreting cells (α-cells), which secrete glucagon in response to hypoglycemia. The objective of this study was to determine whether OGT is necessary for the regulation of α-cell mass and function in vivo. We utilized genetic manipulation to produce two α-cell specific OGT-knockout models: a constitutive glucagon-Cre (αOGT
Identifiants
pubmed: 33460647
pii: S0021-9258(21)00066-1
doi: 10.1016/j.jbc.2021.100297
pmc: PMC7949098
pii:
doi:
Substances chimiques
Blood Glucose
0
Foxa2 protein, mouse
0
Hepatocyte Nuclear Factor 3-beta
135845-92-0
Pyruvic Acid
8558G7RUTR
Glucagon
9007-92-5
N-Acetylglucosaminyltransferases
EC 2.4.1.-
Ogt protein, mouse
EC 2.4.1.255
Cre recombinase
EC 2.7.7.-
Integrases
EC 2.7.7.-
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
100297Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK115720
Pays : United States
Organisme : NIDDK NIH HHS
ID : R21 DK112144
Pays : United States
Organisme : NICHD NIH HHS
ID : R21 HD100840
Pays : United States
Organisme : NIDDK NIH HHS
ID : T32 DK007203
Pays : United States
Informations de copyright
Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Conflicts of interest The authors have declared that no conflict of interest exists.
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