Circulating MicroRNA-15a Associates With Retinal Damage in Patients With Early Stage Type 2 Diabetes

Elena Sangalli1, Elena Tagliabue1, Lucia La Sala1

  • 1IRCCS MultiMedica, Milan, Italy.

Insights

Plasma microRNA-15a levels are elevated in individuals with impaired glucose tolerance and type 2 diabetes mellitus (T2DM). Higher microRNA-15a is linked to early retinal damage, suggesting its potential as a biomarker for T2DM complications.

Area of Science:

  • Biochemistry
  • Ophthalmology
  • Endocrinology

Background:

  • Circulating microRNAs (miRNAs) show promise as biomarkers for type 2 diabetes mellitus (T2DM) and its complications.
  • Early detection of retinal damage in T2DM is crucial for preventing vision loss.

Purpose of the Study:

  • To investigate the association between microRNA-15a and early retinal damage in individuals with T2DM.
  • To explore microRNA-15a as a potential biomarker for preclinical T2DM and associated retinopathy.

Main Methods:

  • Plasma samples from normal glucose tolerance (NGT), impaired glucose tolerance (IGT), and T2DM subjects were analyzed for microRNA-15a levels using real-time PCR.
  • Ganglion cell complex (GCC) thickness, an early indicator of retinal damage, was measured using Optical Coherence Tomography.
  • Associations between microRNA-15a levels, clinical parameters, and GCC thickness were evaluated.

Main Results:

  • MicroRNA-15a levels were significantly higher in IGT and T2DM groups compared to NGT.
  • MicroRNA-15a levels correlated with body mass index and diabetes biomarkers (fasting glucose, HbA1c, HOMA-IR).
  • Reduced GCC thickness was observed in IGT and T2DM subjects; microRNA-15a correlated with GCC thickness, particularly EV-associated microRNA-15a in T2DM patients.

Conclusions:

  • Plasma microRNA-15a levels are elevated in individuals with glucose intolerance and T2DM.
  • MicroRNA-15a, especially EV-associated forms, may serve as a biomarker for early retinal damage in T2DM.
  • Assessing plasma microRNA-15a could aid in risk stratification and secondary prevention strategies for preclinical T2DM.

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