Thymosin Beta 4 (TB-500)


 

2mg Vial
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Synonyms Thymosin Beta 4
Molecular Formula C212H350N56O78S
Molecular Weight 4863.49
Sequence Ac-Ser-Asp-Lys-Pro-Asp-Met-Ala-Glu-Ile-Glu-Lys-Phe-Asp-Lys-Ser-Lys-Leu-Lys-Lys-Thr-Glu-Thr-Gln-Glu-Lys-Asn-Pro-Leu-Pro-Ser-Lys-Glu-Thr- Ile-Glu-Gln-Glu-Lys-Gln-Ala-Gly-Glu-Ser-OH
Appearance White Powder
Purity >98%(HPLC)
Identity (ESI-MS) 4863±5.1
Source Chemical Synthesis
Bacterial Endotoxins < 5EU/mg
Test Parameter Standard
Solubility Soluble in water or 1% acetic acid
Storage Lyophilized Thymosin Beta 4(TB500) although stable at room temperature for 3 weeks, should be stored desiccated below -18°C. Upon reconstitution FST should be stored at 4°C between 2-7 days and for future use below -18°C.
Thymosin beta 4 ameliorates hyperglycemia and improves insulin resistance of KK Cg-Ay/J mouse
Insulin resistance is a key feature of type 2 diabetes mellitus and is also associated with an increased risk of cardiovascular disease (CVD) [1-3]. There are lots of drugs in the market which aim to improve insulin resistance. However, besides metformin, other drugs have had serious adverse effects and have either been withdrawn from the market or subjected to serious warnings. For instance, rosiglitazone, an insulin sensitizer which acts by binding to the PPAR receptors in fat cells and making the cells more responsive to insulin, has been found to be associated with an increased risk of heart attack [4]. Thus, it is very necessary to explore novel potential insulin sensitizers which could not only improve the insulin resistance but also decrease the risk of cardiovascular disease.

Thymosin Beta 4 (Tβ4) is a major intracellular G-actin-sequestering peptide. Previous studies have showed that Tβ4 levels decreased significantly in corneas of diabetic patients compared with healthy subjects [5], and exogenous Tβ4 administration would promote wound healing in diabetic and nondiabetic corneas [6,7]. Therefore, this study was designed to determine the role of Tβ4 on glucose tolerance and hyperinsulinaemia in a KK Cg – Ay/J (KK) mouse model of type 2 diabetes mellitus.

All KK mice were purchased from the Jackson Laboratory and C57BL mice were obtained from the Animal Resources Centre, NUS. In this study, non-diabetic C57BL mice were used as normal control. KK mice were divided into the following groups: KK control group with saline treatment; KK Tβ4 group with daily Tβ4 100 ng/10 g body weight intraperitoneal injection for 12 weeks. The phosphorylated AKT and total AKT protein levels of skeletal muscle from all groups were determined. OGTT, Tβ4, plasma insulin, HbA1c, serum adiponectin, cholesterol, and triglyceride were measured before and after Tβ4 treatment.

Figure 1.
 

The plasma Tβ4 concentrations increased slightly to 6.00 ± 0.45 μg/ml in C57BL Tβ4 group and 2.94 ± 0.23 μg/ml in KK Tβ4 group. However, the statistical difference between concentration at baseline and that after 12 weeks treatment both in C57BL and KK mice was not significant.

Figure 2.
 

As shown in Figure 2.A, KK mice developed hyperglycemia and glucose intolerance at 12-14 weeks old, and glucose concentrations of two KK groups were significantly higher than those in the C57BL groups. In Figure 2.B & C, KK control group remained hyperglycemic and glucose intolerant at 6 weeks after saline treatment, and still had severe hyperglycemia and glucose intolerance at 12 weeks after saline treatment. As shown in Figure 2.D, KK mice developed hyperinsulinaemia at 12-14 weeks of age, and remained it at 6 weeks after Tβ4 treatment. Plasma insulin concentrations of KK groups were significantly higher than those in the C57BL groups. At 12 weeks after saline or Tβ4 treatment, KK control group mice remained severely hyperinsulinaemia.

Table 1.
 

Table 1 show that results of the fasting plasma metabolites. Fasting insulin and triglyceride in the two KK groups were significantly higher than those of C57BL groups at 12 to 14 weeks old. AT 6 weeks after Tβ4 treatment, they were still higher in the two KK groups than those of C57BL groups. At 12 weeks after saline treatment, the fasting insulin levels of KK control mice have increased, while KK Tβ4 group remained unchanged.

Figure 3.
 

As the data shown in figure 3, Tβ4 treatment increased AKT activity in response to glucose challenge, which might lead to increased uptake of glucose by skeletal muscles.

Figure 4.
 

The blood glucose level in KK Tβ4 group was lower than that in KK control group. The average insulin level of KK Tβ4 group was lower than the counterpart of KK control group. However, the difference between them did not reach statistical significance.

In conclusion, the preliminary data indicates that Tβ4 could improve glucose intolerance and ameliorated insulin resistance in KK mouse. Moreover, Tβ4 may be a potential alternative insulin sensitizer for the treatment of type 2 diabetes mellitus.

References

1. Chen G, Lai X, Jiang Q, Chen F, Chen N, Huang H, et al. Cardiovascular disease (CVD) risk, insulin resistance and beta-cell function in prehypertension population of China. Atherosclerosis 2011;217:279–85.

2. Godsland IF, Lecamwasam K, Johnston DG. A systematic evaluation of the insulin resistance syndrome as an independent risk factor for cardiovascular disease mortality and derivation of a clinical index. Metabolism 2011;60:1428–42.

3. Reddy KJ, Singh M, Bangit JR, Batsell RR. The role of insulin resistance in the pathogenesis of atherosclerotic cardiovascular disease: an updated review. J Cardiovasc Med (Hagerstown) 2010;11:633–47.

4. Winterstein AG. Rosiglitazone and the risk of adverse cardiovascular outcomes. Clin Pharmacol Ther 2011;89:776–8.

5. Saghizadeh M, Kramerov AA, Tajbakhsh J, Aoki AM, Wang C, Chai NN, et al. Proteinase and growth factor alterations revealed by gene microarray analysis of human diabetic corneas. Invest Ophthalmol Vis Sci 2005;46:3604–15.

6. Sosne G, Qiu P, Kurpakus-Wheater M, Matthew H. Thymosin beta4 and corneal wound healing: visions of the future. Ann N Y Acad Sci 2010; 1194:190–8.

7. Dunn SP, Heidemann DG, Chow CY, Crockford D, Turjman N, Angel J, et al. Treatment of chronic nonhealing neurotrophic corneal epithelial defects with Thymosin beta4. Ann N Y Acad Sci 2010; 1194: 199–206.

For Research Purpose only, Not for Human Consumption