Towards better understanding of the contributions of overwork and glucotoxicity to the β-cell inadequacy of type 2 diabetes

G. C. Weir, L. Marselli, P. Marchetti, H. Katsuta, M. H. Jung, S. Bonner-Weir

研究成果: Contribution to journalArticle査読

76 被引用数 (Scopus)

抄録

Type 2 diabetes (T2D) is characterized by reduction of β-cell mass and dysfunctional insulin secretion. Understanding β-cell phenotype changes as T2D progresses should help explain these abnormalities. The normal phenotype should differ from the state of overwork when β-cells compensate for insulin resistance to keep glucose levels normal. When only mild hyperglycaemia develops, β-cells are subjected to glucotoxicity. As hyperglycaemia becomes more severe, so does glucotoxicity. β-Cells in all four of these situations should have separate phenotypes. When assessing phenotype with gene expression, isolated islets have artefacts resulting from the trauma of isolation and hypoxia of islet cores. An advantage comes from laser capture microdissection (LCM), which obtains β-cell-rich tissue from pancreatic frozen sections. Valuable data can be obtained from animal models, but the real goal is human β-cells. Our experience with LCM and gene arrays on frozen pancreatic sections from cadaver donors with T2D and controls is described. Although valuable data was obtained, we predict that the approach of taking fresh samples at the time of surgery is an even greater opportunity to markedly advance our understanding of how β-cell phenotype evolves as T2D develops and progresses.

本文言語英語
ページ(範囲)82-90
ページ数9
ジャーナルDiabetes, Obesity and Metabolism
11
SUPPL. 4
DOI
出版ステータス出版済み - 11 2009
外部発表はい

All Science Journal Classification (ASJC) codes

  • 内科学
  • 内分泌学、糖尿病および代謝内科学
  • 内分泌学

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