Abstract

The imprinting control region (ICR) is a region that controls imprinted expression of Igf2/H19 so that Igf2 will only be expressed from the paternal allele instead of the maternal allele. This research aimed to reveal if ICR methylation status’ change contributes to the emergence of type II diabetes Mellitus (T2DM) throughout the induction in mice model. The methylation changes were detected by methylation-specific PCR (MSP). The Control group was given a normal diet and buffer vehicle injection while treatment group was given a high fat diet (HFD) and six times 60 mg/kg mice body weight streptozotocin injection. The induction process was conducted for 12 weeks. The insulin tolerance test (ITT) was conducted on week 0, week 9, and week 12. The treatment’s mice group was successfully induced a significantly higher area under the curve (AUC) compared to the control mice (P < 0, 05). Moreover, ITT showed that diabetic induced mice had higher glucose levels at every time point of the test. Meanwhile, there were no evident ICR methylation changes through week 0 to week 12. Thus, ICR methylation is not proven to contribute to the emergence of T2DM.

Highlights

  • The clinical symptom of diabetes mellitus type II (T2DM) includes when a person experiences an increase in blood sugar without a normal response to lower the levels back

  • The imprinting control region (ICR) is a region that controls imprinted expression of Igf2/H19 so that Igf2 will only be expressed from the paternal allele instead of the maternal allele

  • ICR methylation is not proven to contribute to the emergence of T2DM

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Summary

Introduction

The clinical symptom of diabetes mellitus type II (T2DM) includes when a person experiences an increase in blood sugar without a normal response to lower the levels back. This condition could be preceded by a decrease in insulin receptor sensitivity, which causes insulin resistance. Igf overexpression could increase pancreatic beta cells to damage, leading to the pathophysiology of T2DM [4]. It is unknown whether these changes in T2DM progression cause or effect T2DM

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