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

Diabetologia. 2012 Nov;55(11):2985-8. doi: 10.1007/s00125-012-2666-2. Epub 2012 Jul 31.

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Animals
  • Blood Glucose / metabolism
  • Cell Nucleus / metabolism
  • Cells, Cultured
  • Diabetes Mellitus, Type 2 / metabolism*
  • Diabetes Mellitus, Type 2 / physiopathology*
  • Embryonic Stem Cells / cytology
  • Embryonic Stem Cells / metabolism
  • Female
  • Glucagon / metabolism
  • Humans
  • Hyperglycemia / metabolism
  • Hyperglycemia / physiopathology
  • Insulin / metabolism
  • Insulin Secretion
  • Insulin-Secreting Cells / physiology*
  • Maf Transcription Factors, Large / deficiency*
  • Maf Transcription Factors, Large / metabolism
  • Male
  • Middle Aged
  • Rats
  • Rats, Nude

Substances

  • Blood Glucose
  • Insulin
  • MAFA protein, human
  • Maf Transcription Factors, Large
  • Glucagon