Recovery of islet beta-cell function in streptozotocin- induced diabetic mice: an indirect role for the spleen.

Yin D, Tao J, Lee DD, Shen J, Hara M, Lopez J, Kuznetsov A, Philipson LH, Chong AS
Diabetes. 2006 55 (12): 3256-63

PMID: 17130468 · DOI:10.2337/db05-1275

Limitations in islet beta-cell transplantation as a therapeutic option for type 1 diabetes have prompted renewed interest in islet regeneration as a source of new islets. In this study we tested whether severely diabetic adult C57BL/6 mice can regenerate beta-cells. Diabetes was induced in C57BL/6 mice with high-dose streptozotocin (160-170 mg/kg). In the absence of islet transplantation, all diabetic mice remained diabetic (blood glucose >400 mg/dl), and no spontaneous reversal of diabetes was observed. When syngeneic islets (200/mouse) were transplanted into these diabetic mice under a single kidney capsule, stable restoration of euglycemia for >/=120 days was achieved. Removal of the kidney bearing the transplanted islets at 120 days posttransplantation revealed significant restoration of endogenous beta-cell function. This restoration of islet function was associated with increased beta-cell mass, as well as beta-cell hypertrophy and proliferation. The restoration of islet cell function was facilitated by the presence of a spleen; however, the facilitation was not due to the direct differentiation of spleen-derived cells into beta-cells. This study supports the possibility of restoring beta-cell function in diabetic individuals and points to a role for the spleen in facilitating this process.

MeSH Terms (12)

Animals Blood Glucose Cell Differentiation Diabetes Mellitus, Experimental Glucose Tolerance Test Insulin-Secreting Cells Kinetics Mice Mice, Inbred C57BL Reference Values Spleen Time Factors

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