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. 2011 Apr 6;13(4):440-449.
doi: 10.1016/j.cmet.2011.02.012.

Control of pancreatic β cell regeneration by glucose metabolism

Shay Porat  1 , Noa Weinberg-Corem  2 , Sharona Tornovsky-Babaey  3 , Rachel Schyr-Ben-Haroush  4 , Ayat Hija  2 , Miri Stolovich-Rain  2 , Daniela Dadon  2 , Zvi Granot  2 , Vered Ben-Hur  5 , Peter White  6 , Christophe A Girard  7 , Rotem Karni  5 , Klaus H Kaestner  6 , Frances M Ashcroft  7 , Mark A Magnuson  8 , Ann Saada  9 , Joseph Grimsby  10 , Benjamin Glaser  11 , Yuval Dor  12
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Free article

Control of pancreatic β cell regeneration by glucose metabolism

Shay Porat et al. Cell Metab. .
Free article

Abstract

Recent studies revealed a surprising regenerative capacity of insulin-producing β cells in mice, suggesting that regenerative therapy for human diabetes could in principle be achieved. Physiologic β cell regeneration under stressed conditions relies on accelerated proliferation of surviving β cells, but the factors that trigger and control this response remain unclear. Using islet transplantation experiments, we show that β cell mass is controlled systemically rather than by local factors such as tissue damage. Chronic changes in β cell glucose metabolism, rather than blood glucose levels per se, are the main positive regulator of basal and compensatory β cell proliferation in vivo. Intracellularly, genetic and pharmacologic manipulations reveal that glucose induces β cell replication via metabolism by glucokinase, the first step of glycolysis, followed by closure of K(ATP) channels and membrane depolarization. Our data provide a molecular mechanism for homeostatic control of β cell mass by metabolic demand.

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