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Diabetologia
Published in: Diabetologia 11/2012

01-11-2012 | Short Communication

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

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

Published in: Diabetologia | Issue 11/2012

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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 non-diabetic 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.
Literature
1.
Robertson RP (2004) Chronic oxidative stress as a central mechanism for glucose toxicity in pancreatic islet beta cells in diabetes. J Biol Chem 279:42351–42354PubMedCrossRef
2.
Harmon JS, Stein R, Robertson RP (2005) Oxidative stress-mediated, post-translational loss of MafA protein as a contributing mechanism to loss of insulin gene expression in glucotoxic beta cells. J Biol Chem 280:11107–11113PubMedCrossRef
3.
Wang H, Brun T, Kataoka K, Sharma AJ, Wollheim CB (2007) MAFA controls genes implicated in insulin biosynthesis and secretion. Diabetologia 50:348–358PubMedCrossRef
4.
Harmon JS, Bogdani M, Parazzoli SD et al (2009) Beta-cell-specific overexpression of glutathione peroxidase preserves intranuclear MafA and reverses diabetes in db/db mice. Endocrinology 150:4855–4862PubMedCrossRef
5.
Zhang C, Moriguchi T, Kajihara M et al (2005) MafA is a key regulator of glucose-stimulated insulin secretion. Mol Cell Biol 25:4969–4976PubMedCrossRef
6.
Nishimura W, Kondo T, Salameh T et al (2006) A switch from MafB to MafA expression accompanies differentiation to pancreatic beta-cells. Dev Biol 293:526–539PubMedCrossRef
7.
Matveyenko AV, Georgia S, Bhushan A, Butler PC (2010) Inconsistent formation and nonfunction of insulin-positive cells from pancreatic endoderm derived from human embryonic stem cells in athymic nude rats. Am J Physiol Endocrinol Metab 299:E713–E720PubMedCrossRef
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Dai C, Brissova M, Hang Y et al (2012) Islet-enriched gene expression and glucose-induced insulin secretion in human and mouse islets. Diabetologia 55:707–718PubMedCrossRef
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Salomon D, Meda P (1986) Heterogeneity and contact-dependent regulation of hormone secretion by individual B cells. Exp Cell Res 162:507–520PubMedCrossRef
Metadata
Title
Beta cell nuclear musculoaponeurotic fibrosarcoma oncogene family A (MafA) is deficient in type 2 diabetes
Authors
A. E. Butler
R. P. Robertson
R. Hernandez
A. V. Matveyenko
T. Gurlo
P. C. Butler
Publication date
01-11-2012
Publisher
Springer-Verlag
Published in
Diabetologia / Issue 11/2012
Print ISSN: 0012-186X
Electronic ISSN: 1432-0428
DOI
https://doi.org/10.1007/s00125-012-2666-2

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