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|Title:||Thymosin beta 4 ameliorates hyperglycemia and improves insulin resistance of KK Cg-Ay/J mouse||Authors:||Zhu, J.
Thymosin beta 4
|Issue Date:||Apr-2012||Citation:||Zhu, J., Su, L.-P., Ye, L., Lee, K.-O., Ma, J.-H. (2012-04). Thymosin beta 4 ameliorates hyperglycemia and improves insulin resistance of KK Cg-Ay/J mouse. Diabetes Research and Clinical Practice 96 (1) : 53-59. ScholarBank@NUS Repository. https://doi.org/10.1016/j.diabres.2011.12.009||Abstract:||Object: To evaluate the efficacy of thymosin beta 4 (Tβ 4) on hyperglycemia and insulin sensitivity in a mouse model of type 2 diabetes mellitus (T2DM). Methods: KK mice were divided into the following groups: KK control group, with saline treatment; KK Tβ 4 group, with daily Tβ 4 100ng/10g body weight intraperitoneal injection for 12 weeks. Non-diabetic C57BL mice were used as normal control. OGTT, plasma insulin, HbA1c, serum adiponectin, Tβ 4, cholesterol, and triglyceride were measured before and after Tβ 4 treatment. The phosphorylated AKT and total AKT protein levels of skeletal muscle from all groups were determined. Results: After Tβ 4 treatment, repeat OGTT showed a significant decrease in glucose profiles in the KK Tβ 4 group compared with the KK control group. The KK-Tβ 4 group had reduced mean HbA1c and triglyceride levels, and increased adiponectin compared with KK control group. C57BL mice showed normal glucose homeostasis. The phosphorylated AKT levels of skeletal muscle were significantly increased in KK Tβ 4 group compared with KK control group after glucose stimulation. C57BL mice showed no changes in phosphorylated AKT levels after Tβ 4 treatment. Conclusions: Tβ 4 improved glucose intolerance and ameliorated insulin resistance in KK mouse. Tβ 4 may be a potential alternative insulin sensitizer for treatment of T2DM. © 2011 Elsevier Ireland Ltd.||Source Title:||Diabetes Research and Clinical Practice||URI:||http://scholarbank.nus.edu.sg/handle/10635/88183||ISSN:||01688227||DOI:||10.1016/j.diabres.2011.12.009|
|Appears in Collections:||Staff Publications|
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