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- Title
Skeletal Myoblast Transplantation for Improvement of Hyperglycemia and Insulin Sensitivity.
- Authors
Lei Ye; Lee, Kok O.; Toh, Wee C.; Haider, Husnain K.; Law, Peter K.; Su, Li P.; Wei Zhang; Sim, Eugene K.
- Abstract
Aim: Type II diabetes mellitus is characterized by hyperglycemia and insulin resistance. The study is to investigate the feasibility and efficacy of skeletal myoblast transplantation for attenuation of hyperglycemia and improvement of insulin sensitivity on type II diabetes in a mouse model. Methods: KK Cg-A[sup y]/J mice (Type II diabetes model) aged 12-14 weeks after screening (fasting glucose> 6.4 mmol/L and glucose > 13 mmol/L at 2-hour of fasting glucose tolerance test) were divided into two groups: control group-1 (n=10): receiving 1.5 ml DMEM only, and experimental group-2 (n=10): receiving 1.5 ml DMEM with human skeletal myoblast (HSM) labeled with 4,6-diamidino-2-phenylindole (DAPI). HSM was intramuscularly injected into the both lower limb muscles of KK Cg-A[sup y]/J mice. Fasting glucose tolerance test were performed at before and 12 weeks after treatment. Fasting serum adiponectin, HbA1c, insulin and triglyceride were determined. Results: Histochemical study demonstrated extensive survival of HSM in the skeletal muscles of HSM transplanted group-2 at 12 weeks. Intra-peritoneal glucose tolerance test showed significantly reduced glucose (0 hour = 4.28±0.61, 0.5 hour= 10.57±1.46, 1 hour= 10.24±1.35, 2 hour = 5.57±0.64) compared to controls (0 hour=6.74±0.63, 0.5 hour= 17.22±1.53, 1 hour=19.37±2.28, 2 hour=12.52±2.12) at 12 weeks after HSM transplantation (p<0.05; ANOVA repeated measures). Fasting adiponectin, HbA1c, insulin and triglyceride in experimental group-2 (4.7±0.4ng/ml, 4.4±0.72%, 0.635±0.31 ng/ml, 3.59±0.19mmol/L, respectively) were significantly higher or lower (p<0.05) than those of control group- 1 (3.18±0.52 ng/ml, 5.45±0.2%, 0.93±0.27ng/ml, 4.93±0.16mmol/L) at 12 weeks after treatment. Conclusion: Skeletal myoblast transfer therapy improved glucose tolerance and insulin sensitivity in a Type II diabetes mouse model. This approach may be served as an alternative treatment for insulin resistance of skeletal muscle.
- Publication
Diabetes, 2007, Vol 56, pA524
- ISSN
0012-1797
- Publication type
Academic Journal