4.5 Article

Loss of Foxd3 Results in Decreased β-Cell Proliferation and Glucose Intolerance During Pregnancy

期刊

ENDOCRINOLOGY
卷 152, 期 12, 页码 4589-4600

出版社

ENDOCRINE SOC
DOI: 10.1210/en.2010-1462

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资金

  1. Vanderbilt Diabetes Research and Training Center [P60 DK020593]
  2. Vanderbilt University [P60 DK020593, P60 DK59637]
  3. Juvenile Diabetes Research Foundation [1-2006-219]
  4. National Institutes of Health [RO1 HD036720]
  5. Vanderbilt University Medical Center
  6. Molecular Endocrinology Training Program Grant [T32 DK07563-10]
  7. American Heart Association [10PRE4500024]
  8. [U19 DK042502]

向作者/读者索取更多资源

A complete molecular understanding of beta-cell mass expansion will be useful for the improvement of therapies to treat diabetic patients. During normal periods of metabolic challenges, such as pregnancy, beta-cells proliferate, or self-renew, to meet the new physiological demands. The transcription factor Forkhead box D3 (Foxd3) is required for maintenance and self-renewal of several diverse progenitor cell lineages, and Foxd3 is expressed in the pancreatic primordium beginning at 10.5 d postcoitum, becoming localized predominantly to beta-cells after birth. Here, we show that mice carrying a pancreas-specific deletion of Foxd3 have impaired glucose tolerance, decreased beta-cell mass, decreased beta-cell proliferation, and decreased beta-cell size during pregnancy. In addition, several genes known to regulate proliferation, Foxm1, Skp2, Ezh2, Akt2, and Cdkn1a, are misregulated in islets isolated from these Foxd3 mutant mice. Together, these data place Foxd3 upstream of several pathways critical for beta-cell mass expansion in vivo. (Endocrinology 152: 4589-4600, 2011)

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