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β-Cell Expansion for Therapeutic Compensation of Insulin Resistance in Type 2 Diabetes

By Shimon Efrat


Insulin resistance is the primary cause of type 2 diabetes. However, if compensated by increased insulin production, insulin resistance by itself does not lead to overt disease. Type 2 diabetes develops when this compensation is insufficient, due to defects in β-cell function and in regulation of the β-cell mass. β-Cell transplantation, as well as approaches that replenish or preserve the endogenous β-cell mass, may facilitate the treatment of type 2 diabetes in patients requiring exogenous insulin

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    1. A.B.,andCornelius,J.G.(2000)Reversalofinsulin-dependent diabetes using islets generated in vitro from pancreatic stem cells.
    2. (1995). and patients with NIDDM.
    3. andPortha,B.(2002)Persistentimprovementoftype2diabetes in the Goto-Kakizaki rat model by expansion of the beta-cell mass during the prediabetic period with glucagon-like peptide1 or exendin-4.
    4. (2003). Beta-cell deficit and increased beta-cell apoptosis in humans with type 2 diabetes.
    5. (2001). Beta-cell differentiation from a human pancreatic cell line in vitro and in vivo.
    6. (2002). Clonal identification and characterization of self-renewing pluripotent stem cells in the developing liver.
    7. (2002). Combined expression of pancreatic duodenal homeobox 1 and islet factor 1 induces immature enterocytes to produce insulin.
    8. (1995). Conditional transformation of a pancreatic ¯-celllinederivedfromtransgenicmiceexpressingatetracyclineregulated oncogene.
    9. (2001). Correction ofhyperglycemiaindiabeticmicetransplantedwithreversiblyimmortalized pancreatic ¯ cells controlled by the tet-on regulatory system.
    10. (2001). Differentiation of embryonic stem cells to insulin-secretingstructuressimilartopancreaticislets.Science,
    11. (1995). Duct-toislet-celldifferentiationandisletgrowthinthepancreasofductligated adult rats.
    12. (1995). Dynamicsofbeta-cellmassinthegrowingratpancreas.Estimation with a simple mathematical model.
    13. (2000). Engineering the pancreatic ¯-cell. In: Diabetes Mellitus: A Fundamental and Clinical Text,
    14. (1998). Functional analysis of a conditionally-transformed pancreatic ¯-cell line.
    15. (2002). Growth inhibitors promote differentiation of insulin-producingtissuefromembryonicstemcells.Proc.Natl.
    16. (2000). In vitro cultivation of human islets from expanded ductal tissue.
    17. (2002). In vitro transdifferentiation of adult hepatic stem cells into pancreatic endocrine hormone-producing cells.
    18. (2001). Insulin production by human embryonic stem cells.
    19. (2000). Insulin-secreting cells derived from embryonic stem cells normalize glycemia in streptozotocin-induced diabetic mice.
    20. (1990). Natural history of beta-cell dysfunction in NIDDM.
    21. (2000). Pancreatic and duodenal homeobox gene 1¯-CELL
    22. (2001). Regulation of beta-cell mass by hormones and growth factors.
    23. (1999). resulting in increased beta-cell mass and improved glucose tolerance in diabetic rats.
    24. (1999). The glucagon-like peptides.
    25. W.C.,Largaespada,D.A.,andVerfaillie,C.M.(2002)Pluripotency of mesenchymal stem cells derived from adult marrow.

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