MicroRNA 144 Impairs Insulin Signaling by Inhibiting the Expression of Insulin Receptor Substrate 1 in Type 2 Diabetes Mellitus
2011

MicroRNA 144 Impairs Insulin Signaling in Type 2 Diabetes

Sample size: 50 publication 10 minutes Evidence: moderate

Author Information

Author(s): Karolina Dwi Setyowati, Armugam Arunmozhiarasi, Tavintharan Subramaniam, Wong Michael T. K., Lim Su Chi, Sum Chee Fang, Jeyaseelan Kandiah

Primary Institution: National University of Singapore

Hypothesis

The study investigates the role of circulating microRNAs, particularly miR-144, as biomarkers and regulators in Type 2 Diabetes Mellitus.

Conclusion

The study identifies miR-144 as a significant modulator of insulin receptor substrate 1 (IRS1), suggesting its potential as a biomarker for Type 2 Diabetes.

Supporting Evidence

  • miR-144 was found to be highly up-regulated in Type 2 Diabetes patients.
  • Increased levels of circulating miR-144 correlated with decreased IRS1 expression.
  • miR-144 directly targets IRS1, inhibiting its expression.
  • Eight miRNAs were identified as potential biomarkers for distinguishing between impaired fasting glucose and Type 2 Diabetes.

Takeaway

This study found that a tiny molecule called miR-144 can make it harder for the body to use insulin, which is important for controlling blood sugar levels.

Methodology

The study used miRNA microarray and stem-loop real-time RT-PCR to analyze miRNA expression in blood and tissues from Type 2 Diabetes rat models and human patients.

Potential Biases

Potential bias in participant selection as all subjects were not on any medications and were newly diagnosed.

Limitations

The study primarily focused on male participants and may not be generalizable to females or other populations.

Participant Demographics

The study included 50 male participants with a mean age of 40.5 years, categorized into healthy controls, impaired fasting glucose, and Type 2 Diabetes groups.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0022839

Want to read the original?

Access the complete publication on the publisher's website

View Original Publication