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Diabetes. 2017 Aug;66(8):2092-2101. doi: 10.2337/db16-1213. Epub 2017 May 15.

Pair Feeding, but Not Insulin, Phloridzin, or Rosiglitazone Treatment, Curtails Markers of β-Cell Dedifferentiation in db/db Mice.

Author information

1
Department of Medicine and Naomi Berrie Diabetes Center, Columbia University, New York, New York.
2
Department of Medicine and Naomi Berrie Diabetes Center, Columbia University, New York, New York da230@cumc.columbia.edu.

Abstract

β-Cell failure is a hallmark of type 2 diabetes. Among several cellular biological mechanisms of cellular dysfunction, we and others have recently proposed that dedifferentiation of β-cells can explain the slowly progressive onset and partial reversibility of β-cell failure. Accordingly, we provided evidence of such processes in humans and experimental animal models of insulin-resistant diabetes. In this study, we asked whether β-cell dedifferentiation can be prevented with diet or pharmacological treatment of diabetes. db/db mice, a widely used model of insulin-resistant diabetes and obesity, were either pair fed or treated with the Sglt inhibitor phloridzin, the insulin-sensitizer rosiglitazone, or insulin. All treatments were equally efficacious in reducing plasma glucose levels. Pair feeding and phloridzin also resulted in significant weight loss. However, pair feeding among the four treatments resulted in a reduction of β-cell dedifferentiation, as assessed by Foxo1 and Aldh1a3 immunohistochemistry. The effect of diet to partly restore β-cell function is consistent with data in human diabetes and provides another potential mechanism by which lifestyle changes act as an effective intervention against diabetes progression.

PMID:
28506962
PMCID:
PMC5521857
[Available on 2018-08-01]
DOI:
10.2337/db16-1213
[Indexed for MEDLINE]
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