C57BL/6J mice (wild type, Japan CLEA, Osaka, Japan) and C57BL/6-Tg (UBC-GFP) 30Scha/J mice (GFP-Tg mice, The Jackson Laboratory, Bar Harbor, ME) were used. Hyperglycemia was induced by intravenous injection of streptozotocin (STZ) (150 mg/kg) (Nacalai Tesque, Kyoto, Japan) to create the type 1 diabetic model (STZ mice) or by feeding a highfat diet (HFD) (Oriental bio service, Osaka, Japan) tocreate the type 2 diabetic model (HFD mice). Mice injected with buffer alone or fed normal chow were used as normoglycemic controls (Ctrl), respectively, for type 1 and type 2. For BMT, we isolated bone marrow cells from 8-week GFP-Tg mice. Wild type mice were irradiated (9 Gy) and injected with 4 × 106 bone marrow cells from GFP-Tg (GFP-BMT mice). Four weeks after BMT, hyperglycemia was induced in GFP-BMT mice by STZ i.v. injection or by feeding a high fat diet. These mice were analyzed 9–12 weeks after STZ injection or the commencement of high fat feeding. Blood glucose levels were measured once a week in all experimental mice. These animals were maintained under standard conditions with a 12:12-h light–dark cycle and provided with standard laboratory chow or high fat diet and water ad libitum.
The Animal Care Committees of Shiga University of Medical Science approved all experimental protocols performed in this study (#2011-7-5HH).
The Animal Care Committees of Shiga University of Medical Science approved all experimental protocols performed in this study (#2011-7-5HH).