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Defective insulin secretion and increased susceptibility to experimental diabetes are induced by reduced Akt activity in pancreatic islet β cells
Open accessAbstract
The insulin and IGF signaling pathways are critical for development and maintenance of pancreatic beta cell mass and function. The serine-threonine kinase Akt is one of several mediators regulated by these pathways. We have studied the role of Akt in pancreatic beta cell physiology by generating transgenic mice expressing a kinase-dead mutant of this enzyme in beta cells. Reduction of Akt activity in transgenic animals resulted in impaired glucose tolerance due to defective insulin secretion. The mechanisms involved in dysregulation of secretion in these mice lie at the level of insulin exocytosis and are not the result of abnormalities in glucose signaling or function of voltage-gated Ca2+ channels. Therefore, transgenic mice showed increased susceptibility to developing glucose intolerance and diabetes following fat feeding. These observations suggest that Akt plays a novel and important role in the regulation of distal components of the secretory pathway and that this enzyme represents a therapeutic target for improvement of beta cell function in diabetes.
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Garofalo, R. S., Orena, S. J., Rafidi, K., Torchia, A. J., Stock, J. L., Hildebrandt, A. L., Coskran, T., Black, S. C., Brees, D. J., Wicks, J. R., et al. (2003) · Journal of Clinical Investigation · doi:10.1172/jci16885 · Cited by 726
Defective insulin secretion in hepatocyte nuclear factor 1alpha-deficient mice.
Pontoglio, M., Sreenan, S., Roe, M., Pugh, W., Ostrega, D., Doyen, A., Pick, A. J., Baldwin, A., Velho, G., Froguel, P., et al. (1998) · Journal of Clinical Investigation · doi:10.1172/jci2548 · Cited by 321 · cited 1×
“experiments were carried out as described previously (39).”
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Research works printed but not linked: 42
- White, 2002, Am. J. Physiol. Endocrinol. Metab., 283, E413, 10.1152/ajpendo.00514.2001 · DOI · Paper page
- 10.1210/jc.86.9.4047 · DOI · Paper page
- 10.1016/S1043-2760(00)00305-2 · DOI · Paper page
- 10.1016/S0092-8674(00)80546-2 · DOI · Paper page
- 10.1172/JCI7917 · DOI · Paper page
- 10.1038/36116 · DOI · Paper page
- Xuan, 2002, J. Clin. Invest., 110, 1011, 10.1172/JCI0215276 · doi:10.1172/jci0215276 · Paper page
- Kulkarni, 2002, Nat. Genet., 31, 111, 10.1038/ng872 · DOI · Paper page
- 10.2337/diabetes.50.10.2237 · DOI · Paper page
- 10.1074/jbc.273.28.17771 · DOI · Paper page
- 10.1042/0264-6021:3440649 · DOI
- 10.1210/en.142.1.229 · DOI
- 10.1006/excr.1999.4690 · DOI · Paper page
- Toker, 2000, Mol. Pharmacol., 57, 652, 10.1124/mol.57.4.652 · doi:10.1124/mol.57.4.652 · Paper page
- 10.1074/jbc.C100462200 · DOI · Paper page
- 10.1101/gad.913901 · DOI · Paper page
- 10.1126/science.292.5522.1728 · DOI · Paper page
- Coffer, 1998, Biochem. J., 335, 1, 10.1042/bj3350001 · DOI · Paper page
- 10.1038/nm1001-1133 · DOI · Paper page
- Bernal-Mizrachi, 2001, J. Clin. Invest., 108, 1631, 10.1172/JCI200113785 · DOI · Paper page
- 10.1074/jbc.271.36.21920 · DOI · Paper page
- 10.1101/gad.11.6.701 · DOI · Paper page
- 10.1126/science.275.5300.661 · DOI · Paper page
- 10.1093/emboj/16.20.6151 · DOI · Paper page
- 10.1016/S0303-7207(00)00324-5 · DOI
- 10.1016/0092-8674(95)90534-0 · DOI · Paper page
- Zhou, 2000, Am. J. Physiol. Endocrinol. Metab., 278, E340, 10.1152/ajpendo.2000.278.2.E340 · DOI
- 10.1172/JCI1245 · DOI
- 10.1074/jbc.M206047200 · DOI · Paper page
- 10.1128/MCB.22.8.2799-2809.2002 · DOI · Paper page
- 10.1074/jbc.M211352200 · DOI
- 10.1046/j.1432-1327.1999.00043.x · DOI · Paper page
- 10.1152/ajpcell.00142.2003 · DOI · Paper page
- 10.1007/s00018-003-3349-4 · DOI
- Kitamura, 2002, J. Clin. Invest., 110, 1839, 10.1172/JCI200216857 · DOI
- 10.1172/JCI116297 · DOI · Paper page
- Johnson, 2003, J. Clin. Invest., 111, 1147, 10.1172/JCI200316537 · DOI
- Roe, 1993, J. Biol. Chem., 268, 9953, 10.1016/S0021-9258(18)82156-1 · DOI
- 10.1073/pnas.222099799 · DOI
- 10.1006/gcen.1999.7349 · doi:10.1006/gcen.1999.7349
- 10.1101/gad.1097103 · DOI · Paper page
- 10.1074/jbc.M401216200 · DOI
Cited by
The PI3K/AKT Pathway in Obesity and Type 2 Diabetes
Huang, X., Liu, G., Guo, J., & Su, Z. (2018) · International Journal of Biological Sciences · doi:10.7150/ijbs.27173 · Cited by 1,673
“In contrast, overexpression of a kinase dead mutant in β cells, which reduced AKT activity by 80%, results in a lack of insulin secretion [145].”
BackgroundTranscription Factor 7-Like 2 Regulates β-Cell Survival and Function in Human Pancreatic Islets
Shu, L., Sauter, N. S., Schulthess, F. T., Matveyenko, A. V., Oberholzer, J., & Maedler, K. (2008) · Diabetes · doi:10.2337/db07-0847 · Cited by 265
RetractedMolecular regulation of pancreatic β-cell mass development, maintenance, and expansion
Ackermann, A. M., & Gannon, M. (2007) · Journal of Molecular Endocrinology · doi:10.1677/jme-06-0053 · Cited by 262
Wijesekara, N., Krishnamurthy, M., Bhattacharjee, A., Suhail, A., Sweeney, G., & Wheeler, M. B. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.085084 · Cited by 229
A causal role for hyperinsulinemia in obesity
Templeman, N. M., Skovsø, S., Page, M. M., Lim, G. E., & Johnson, J. D. (2017) · Journal of Endocrinology · doi:10.1530/joe-16-0449 · Cited by 168
Metadata
- Authors
- Bernal-Mizrachi, E., Fatrai, S., Johnson, J. D., Ohsugi, M., Otani, K., Han, Z., Polonsky, K. S., & Permutt, M. A.
- Venue
- Journal of Clinical Investigation
- Published
- 2004-10-01
- Volume
- 114
- Issue
- 7
- Pages
- 928-936
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2167220221
- Cited by
- 225
- References
- 2
- FWCI
- 8.48
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Bernal-Mizrachi, E., Fatrai, S., Johnson, J. D., Ohsugi, M., Otani, K., Han, Z., Polonsky, K. S., & Permutt, M. A. (2004). Defective insulin secretion and increased susceptibility to experimental diabetes are induced by reduced Akt activity in pancreatic islet β cells. Journal of Clinical Investigation. https://doi.org/10.1172/jci20016
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