The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Control of Pancreatic β Cell Regeneration by Glucose Metabolism
Open accessAbstract
SUMMARY 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 KATP channels and membrane depolarization. Our data provide a molecular mechanism for homeostatic control of β cell mass by metabolic demand.
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Cites
Rejuvenation of aged progenitor cells by exposure to a young systemic environment
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Adult pancreatic β-cells are formed by self-duplication rather than stem-cell differentiation
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Self-citationSelective depletion of macrophages reveals distinct, opposing roles during liver injury and repair
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Molecular and metabolic mechanisms of insulin resistance and β-cell failure in type 2 diabetes
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Conversion of adult pancreatic α-cells to β-cells after extreme β-cell loss
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Nuclear Receptor-Dependent Bile Acid Signaling Is Required for Normal Liver Regeneration
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Recovery from diabetes in mice by β cell regeneration
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Self-citationThe replication of β cells in normal physiology, in disease and for therapy
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Cited by
Beta Cell Dysfunction and Insulin Resistance
Cerf, M. E. (2013) · Frontiers in Endocrinology · doi:10.3389/fendo.2013.00037 · Cited by 964
Decreased consumption of branched-chain amino acids improves metabolic health
Fontana, L., Cummings, N. E., Arriola Apelo, S. I., Neuman, J. C., Kasza, I., Schmidt, B. A., Cava, E., Spelta, F., Tosti, V., Syed, F. A., et al. (2016) · Cell Reports · doi:10.1016/j.celrep.2016.05.092 · Cited by 466
Beta cell hubs dictate pancreatic islet responses to glucose
Johnston, N. R., Mitchell, R. K., Haythorne, E., Pessoa, M. P., Semplici, F., Ferrer, J., Piemonti, L., Marchetti, P., Bugliani, M., Bosco, D., et al. (2016) · Cell Metabolism · doi:10.1016/j.cmet.2016.06.020 · Cited by 454
RETRACTED: Betatrophin: A Hormone that Controls Pancreatic β Cell Proliferation
Yi, P., Park, J.-S., & Melton, D. A. (2013) · Cell · doi:10.1016/j.cell.2013.04.008 · Cited by 449
RetractedPancreatic β Cell Dedifferentiation in Diabetes and Redifferentiation following Insulin Therapy
Wang, Z., York, N. W., Nichols, C. G., & Remedi, M. S. (2014) · Cell Metabolism · doi:10.1016/j.cmet.2014.03.010 · Cited by 406
Metadata
- Authors
- Porat, S., Weinberg-Corem, N., Tornovsky-Babaey, S., Schyr-Ben-Haroush, R., Hija, A., Stolovich-Rain, M., Dadon, D., Granot, Z., Ben-Hur, V., White, P., Girard, C. A., Karni, R., Kaestner, K. H., Ashcroft, F. M., Magnuson, M. A., Saada, A., Grimsby, J., Glaser, B., & Dor, Y.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2011-04
- Volume
- 13
- Issue
- 4
- Pages
- 440-449
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2010561590
- Cited by
- 298
- References
- 12
- FWCI
- 28.63
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Porat, S., Weinberg-Corem, N., Tornovsky-Babaey, S., Schyr-Ben-Haroush, R., Hija, A., Stolovich-Rain, M., Dadon, D., Granot, Z., Ben-Hur, V., White, P., Girard, C. A., Karni, R., Kaestner, K. H., Ashcroft, F. M., Magnuson, M. A., Saada, A., Grimsby, J., Glaser, B., & Dor, Y. (2011). Control of Pancreatic β Cell Regeneration by Glucose Metabolism. Cell Metabolism. https://doi.org/10.1016/j.cmet.2011.02.012
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