Genetic models of Insulin Resistance:Alterations in β-cell biology
作者： Rohit N. Kulkarni , C. Ronald Kahn
DOI: 10.1007/978-1-4615-1669-9_18
关键词: Adipose tissue 、 Cell biology 、 Insulin 、 Polycystic ovarian disease 、 Insulin receptor 、 Genetic model 、 Medicine 、 Insulin receptor substrate 、 Type 2 diabetes 、 Insulin resistance
摘要: One of the essential biological actions insulin in mammals is maintenance euglycaemia. This a complex process and involves uptake, storage oxidation glucose skeletal muscle adipose tissues, as well suppression hepatic production. A significant blunting these spite presence normal or even high circulating levels indicates an “insulin resistant” phenotype. variety pathological states including type 2 diabetes, obesity, hypertension, atherosclerosis polycystic ovary disease are characterized by resistance (1-6). In case diabetes it generally accepted that must be accompanied β-cell defect for full development disease. Although there some debate to which two defects primary, longitudinal studies several populations suggest may first detected (2,7,8). The early observed pre-diabetic individuals initially compensated increase secretion islet β-cells could represent either enhanced secretory capacity increased islet/β-cell mass combination both. Over period time, however, compensation fails leading uncontrolled hyperglycaemia overt diabetes.
springer.com
sci-hub.st 参考文章(110)
R. L. Joshi, B. Lamothe, N. Cordonnier, K. Mesbah, E. Monthioux, J. Jami, D. Bucchini, Targeted disruption of the insulin receptor gene in the mouse results in neonatal lethality. The EMBO Journal. ,vol. 15, pp. 1542- 1547 ,(1996) , 10.1002/J.1460-2075.1996.TB00498.X
C.P. Miller, R.E. McGehee, J.F. Habener, IDX-1: a new homeodomain transcription factor expressed in rat pancreatic islets and duodenum that transactivates the somatostatin gene. The EMBO Journal. ,vol. 13, pp. 1145- 1156 ,(1994) , 10.1002/J.1460-2075.1994.TB06363.X
Sushil G. Rane, Pierre Dubus, Richard V. Mettus, Elizabeth J. Galbreath, Guenther Boden, E. Premkumar Reddy, Mariano Barbacid, Loss of Cdk4 expression causes insulin-deficient diabetes and Cdk4 activation results in beta-islet cell hyperplasia. Nature Genetics. ,vol. 22, pp. 44- 52 ,(1999) , 10.1038/8751
Lawrence S. Phillips, Ching-I Pao, Betty C. Villafuerte, Molecular Regulation of Insulin-like Growth Factor-I and Its Principal Binding Protein, IGFBP-3 Progress in Nucleic Acid Research and Molecular Biology. ,vol. 60, pp. 195- 265 ,(1998) , 10.1016/S0079-6603(08)60894-6
Dominic J. Withers, Deborah J. Burks, Heather H. Towery, Shari L. Altamuro, Carrie L. Flint, Morris F. White, Irs-2 coordinates Igf-1 receptor-mediated β-cell development and peripheral insulin signalling Nature Genetics. ,vol. 23, pp. 32- 40 ,(1999) , 10.1038/12631
M.F. White, C.R. Kahn, The insulin signaling system. Journal of Biological Chemistry. ,vol. 269, pp. 1- 4 ,(1994) , 10.1016/S0021-9258(17)42297-6
M. F. White, L. Yenush, The IRS-signaling system: a network of docking proteins that mediate insulin and cytokine action. Current Topics in Microbiology and Immunology. ,vol. 228, pp. 179- 208 ,(1998) , 10.1007/978-3-642-80481-6_8
Sanjoy Dutta, Susan Bonner-Weir, Marc Montminy, Christopher Wright, Regulatory factor linked to late-onset diabetes? Nature. ,vol. 392, pp. 560- 560 ,(1998) , 10.1038/33311
Dominic J. Withers, Julio Sanchez Gutierrez, Heather Towery, Deborah J. Burks, Jian-Ming Ren, Stephen Previs, Yitao Zhang, Dolores Bernal, Sebastian Pons, Gerald I. Shulman, Susan Bonner-Weir, Morris F. White, Disruption of IRS-2 causes type 2 diabetes in mice Nature. ,vol. 391, pp. 900- 904 ,(1998) , 10.1038/36116
Betty LAMOTHE, Anne BAUDRY, Pierrette DESBOIS, Lucianne LAMOTTE, Danielle BUCCHINI, Pierre DE MEYTS, Rajiv L. JOSHI, Genetic engineering in mice: impact on insulin signalling and action Biochemical Journal. ,vol. 335, pp. 193- 204 ,(1998) , 10.1042/BJ3350193