Endocrine Abstracts

Background: Hyperglycemia and glucose intolerance are perhaps the most common pathophysiologies associated with diabetes. β-Arrestin 2, component of G-protein coupled receptor signaling, has been shown to be down-regulated in insulin resistant and type 2 diabetic mouse models. However, if this down-regulation also existed in diabetic humans, and the possible mechanisms of this differential expression in normal and type 2 diabetes were not clear.

Methods: Venous nucleus cells from normal glucose tolerance subjects and newly-diagnosed type two diabetic patients without any medications were investigated. β-Arrestin 2 mRNA expression were measured by RT-PCR, β-Arrestin 2 DNA promoter methylation was evaluated by MS-PCR. Clinical data of all the subjects were collected.

Results: In diabetic subjects with confirmed insulin resistance, β-Arrestin 2 mRNA was significantly down regulated compared to normal subjects. Tight methylation- regulated CpGs were identified within β-Arrestin 2 promoter area. β-Arrestin 2 promoter methylation were found in diabetic patients but not in the normal subjects.

Conclusion: DNA methylation might be related to the differential expression of β-Arrestin 2 in type 2 diabetes with insulin resistance, and β-Arrestin 2 DNA promotor methylation might contribute to the pathogenesis of type 2 diabetes.

Declaration of interest: I fully declare a conflict of interest. Details below:

Funding: This work was supported, however funding details unavailable.

This work was supported by National Natural Science Foundation of China (No. 30901187).