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

A E Butler1, R P Robertson, R Hernandez

  • 1Larry Hillblom Islet Research Center, UCLA David Geffen School of Medicine, 900 Veteran Avenue, 24-130 Warren Hall, Los Angeles, CA 90095-7073, USA.

Diabetologia
|August 1, 2012
PubMed
Abstract

Insights

Nuclear MafA, crucial for beta cell function, is significantly reduced in humans with type 2 diabetes. This decrease in musculoaponeurotic fibrosarcoma oncogene family A (MafA) may contribute to beta cell dysfunction.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Diabetes Research

Background:

  • The musculoaponeurotic fibrosarcoma oncogene family A (MafA) is a key transcriptional factor regulating genes essential for pancreatic beta cell function.
  • Reduced nuclear MafA levels have been observed in animal models of type 2 diabetes, suggesting a potential role in beta cell dysfunction.

Purpose of the Study:

  • To investigate the abundance of nuclear MafA in pancreatic beta cells of human subjects with and without type 2 diabetes.
  • To determine if reduced nuclear MafA is a characteristic feature of type 2 diabetes in humans.

Main Methods:

  • Human pancreatic tissue samples were obtained from individuals with and without type 2 diabetes.
  • Immunohistochemistry was employed to stain beta cells for insulin, glucagon, and MafA.

Main Results:

  • A significant and marked decrease in nuclear MafA was observed in beta cells from individuals with type 2 diabetes compared to non-diabetic controls (1.6 ± 1.2% vs 46.3 ± 8.3%, p < 0.001).

Conclusions:

  • Nuclear MafA is markedly decreased in pancreatic beta cells of humans with type 2 diabetes.
  • This reduction in nuclear MafA may be a contributing factor to the impaired beta cell function observed in type 2 diabetes.

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