Beta cell nuclear musculoaponeurotic fibrosarcoma oncogene family A (MafA) is deficient in type 2 diabetes

A. E. Butler; R. P. Robertson; R. Hernandez; A. V. Matveyenko; T. Gurlo; P. C. Butler

doi:10.1007/s00125-012-2666-2

Beta cell nuclear musculoaponeurotic fibrosarcoma oncogene family A (MafA) is deficient in type 2 diabetes

A. E. Butler, R. P. Robertson, R. Hernandez, A. V. Matveyenko, T. Gurlo, P. C. Butler

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

Abstract

Aims/hypothesis The beta cell transcriptional factor musculoaponeurotic fibrosarcoma oncogene family A (MafA) regulates genes important for beta cell function. Loss of nuclear MafA has been implicated in beta cell dysfunction in animal models of type 2 diabetes. We sought to establish if nuclear MafA is less abundant in beta cell nuclei in humans with type 2 diabetes. Methods Pancreas obtained at surgery from five nondiabetic individuals and six individuals with type 2 diabetes was immunostained for insulin, glucagon and MafA. Results Beta cell nuclear MafA was markedly decreased in type 2 diabetes (1.6±1.2% vs 46.3±8.3%, p<0.001). Conclusions/interpretation Beta cell nuclear MafA is markedly decreased in humans with type 2 diabetes, which may contribute to impaired beta cell dysfunction.

Original language	English (US)
Pages (from-to)	2985-2988
Number of pages	4
Journal	Diabetologia
Volume	55
Issue number	11
DOIs	https://doi.org/10.1007/s00125-012-2666-2
State	Published - Nov 2012
Externally published	Yes

Keywords

Beta cell
Glucotoxicity
MafA

ASJC Scopus subject areas

Internal Medicine
Endocrinology, Diabetes and Metabolism

Online availability

10.1007/s00125-012-2666-2

Library availability

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title = "Beta cell nuclear musculoaponeurotic fibrosarcoma oncogene family A (MafA) is deficient in type 2 diabetes",

abstract = "Aims/hypothesis The beta cell transcriptional factor musculoaponeurotic fibrosarcoma oncogene family A (MafA) regulates genes important for beta cell function. Loss of nuclear MafA has been implicated in beta cell dysfunction in animal models of type 2 diabetes. We sought to establish if nuclear MafA is less abundant in beta cell nuclei in humans with type 2 diabetes. Methods Pancreas obtained at surgery from five nondiabetic individuals and six individuals with type 2 diabetes was immunostained for insulin, glucagon and MafA. Results Beta cell nuclear MafA was markedly decreased in type 2 diabetes (1.6±1.2% vs 46.3±8.3%, p<0.001). Conclusions/interpretation Beta cell nuclear MafA is markedly decreased in humans with type 2 diabetes, which may contribute to impaired beta cell dysfunction.",

keywords = "Beta cell, Glucotoxicity, MafA",

author = "Butler, {A. E.} and Robertson, {R. P.} and R. Hernandez and Matveyenko, {A. V.} and T. Gurlo and Butler, {P. C.}",

note = "Funding Information: Funding This study was funded by the National Institutes of Health (DK077967, DK059579, DK061539 to PCB and DK032585 to RPR) and the Larry L. Hillblom Foundation.",

year = "2012",

month = nov,

doi = "10.1007/s00125-012-2666-2",

language = "English (US)",

volume = "55",

pages = "2985--2988",

journal = "Diabetologia",

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T1 - Beta cell nuclear musculoaponeurotic fibrosarcoma oncogene family A (MafA) is deficient in type 2 diabetes

AU - Butler, A. E.

AU - Robertson, R. P.

AU - Hernandez, R.

AU - Matveyenko, A. V.

AU - Gurlo, T.

AU - Butler, P. C.

N1 - Funding Information: Funding This study was funded by the National Institutes of Health (DK077967, DK059579, DK061539 to PCB and DK032585 to RPR) and the Larry L. Hillblom Foundation.

PY - 2012/11

Y1 - 2012/11

N2 - Aims/hypothesis The beta cell transcriptional factor musculoaponeurotic fibrosarcoma oncogene family A (MafA) regulates genes important for beta cell function. Loss of nuclear MafA has been implicated in beta cell dysfunction in animal models of type 2 diabetes. We sought to establish if nuclear MafA is less abundant in beta cell nuclei in humans with type 2 diabetes. Methods Pancreas obtained at surgery from five nondiabetic individuals and six individuals with type 2 diabetes was immunostained for insulin, glucagon and MafA. Results Beta cell nuclear MafA was markedly decreased in type 2 diabetes (1.6±1.2% vs 46.3±8.3%, p<0.001). Conclusions/interpretation Beta cell nuclear MafA is markedly decreased in humans with type 2 diabetes, which may contribute to impaired beta cell dysfunction.

AB - Aims/hypothesis The beta cell transcriptional factor musculoaponeurotic fibrosarcoma oncogene family A (MafA) regulates genes important for beta cell function. Loss of nuclear MafA has been implicated in beta cell dysfunction in animal models of type 2 diabetes. We sought to establish if nuclear MafA is less abundant in beta cell nuclei in humans with type 2 diabetes. Methods Pancreas obtained at surgery from five nondiabetic individuals and six individuals with type 2 diabetes was immunostained for insulin, glucagon and MafA. Results Beta cell nuclear MafA was markedly decreased in type 2 diabetes (1.6±1.2% vs 46.3±8.3%, p<0.001). Conclusions/interpretation Beta cell nuclear MafA is markedly decreased in humans with type 2 diabetes, which may contribute to impaired beta cell dysfunction.

KW - Beta cell

KW - Glucotoxicity

KW - MafA

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Beta cell nuclear musculoaponeurotic fibrosarcoma oncogene family A (MafA) is deficient in type 2 diabetes

Abstract

Keywords

ASJC Scopus subject areas

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