The underlying cause of both type 1 and type 2 diabetes is that there are insufficient pancreatic beta-cells to control the level of glucose in the blood.
Given its potential impact on the treatment of diabetes, deciphering the molecular pathways that control beta-cell proliferation is an area of intensive investigation.
In a new study, Anil Bhushan and colleagues from the David Geffen School of Medicine, Los Angeles, show that the protein Skp2 has a critical role in regulating beta-cell proliferation in mice.
The authors observed that mice lacking Skp2 developed more severe insulin resistance and more overt diabetes after being fed a high-fat diet than normal mice. This was associated with decreased degradation of p27 in beta-cells, which prevented the cells from proliferating.
The authors therefore suggest that Skp2-mediated p27 degradation in beta-cells might have a role in regulating beta-cell proliferation in response to metabolic needs.
Article: Essential role of Skp2-mediated p27 degradation in growth and adaptive expansion of pancreatic beta-cells, Journal Of Clinical Investigation
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