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Endothelial Dysfunction in Youth-Onset Type 2 Diabetes: A Clinical Translational Study.

Khaled Z Abd-Elmoniem1, Jehad H Edwan1, Katrina B Dietsche2

  • 1National Institute of Diabetes and Digestive and Kidney Diseases, Biomedical Medical and Imaging Branch (K.Z.A., J.E., N.S., J.M., L.B., W.Q., A.M.G.), National Institutes of Health, Bethesda, MD.

Circulation Research
|July 29, 2024
PubMed
Summary

Youth-onset type 2 diabetes (Y-T2D) causes early coronary and brachial endothelial dysfunction, even without severe risk factors. Plasma vesicles from Y-T2D patients worsen endothelial function, indicating accelerated atherosclerosis.

Keywords:
atherosclerosisbrachial arterycardiovascular diseasesdiabetes, type 2pediatric obesity

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Area of Science:

  • Cardiovascular Research
  • Endocrinology
  • Biomedical Imaging

Background:

  • Youth-onset type 2 diabetes (Y-T2D) increases coronary atherosclerotic disease risk.
  • Early pathological features and cardiac endothelial dysfunction in Y-T2D remain unevaluated.
  • Endothelial function MRI may detect dysfunction before classical risk factors manifest.

Purpose of the Study:

  • Evaluate peripheral and coronary artery structure and endothelial function in young adults with recent Y-T2D.
  • Assess plasma-derived small extracellular vesicles' effects on endothelial cells.
  • Corroborate imaging findings with cellular and molecular analyses.

Main Methods:

  • Utilized endothelial function magnetic resonance imaging (3.0T) to measure coronary and brachial artery function.
  • Analyzed plasma-derived small extracellular vesicles from Y-T2D patients and healthy peers.
  • Treated human coronary artery endothelial cells with Y-T2D plasma-derived small extracellular vesicles, assessing protein expression, oxidative stress, and nitric oxide levels.

Main Results:

  • Y-T2D patients showed greater coronary wall thickness and impaired endothelial function (coronary and brachial).
  • Y-T2D plasma-derived small extracellular vesicles decreased nitric oxide and increased oxidative stress and inflammation in endothelial cells.
  • Hemoglobin A1c and hs-CRP were higher in Y-T2D, but lipid profiles were similar.

Conclusions:

  • Coronary and brachial endothelial dysfunction are evident early in Y-T2D, even without severe hyperglycemia or dyslipidemia.
  • Plasma-derived small extracellular vesicles contribute to endothelial dysfunction markers.
  • Accelerated subclinical coronary atherosclerosis is an early feature of Y-T2D.