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Related Concept Videos

Hyperglycemia01:29

Hyperglycemia

Hyperglycemia is an abnormally high blood glucose level. It is diagnosed by fasting glucose ≥126 mg/dL, 2-hour oral glucose tolerance test (or OGTT) ≥200 mg/dL, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5%. However, HbA1c results may be unreliable in certain conditions, such as anemia or hemoglobinopathies, and the diagnosis should be confirmed unless classic symptoms are present. Postprandial hyperglycemia is typically considered significant when glucose levels exceed 180 mg/dL two...

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Related Experiment Video

Updated: Jun 10, 2026

Drug Treatment by Central Venous Catheter in a Mouse Model of Angiotensin II Induced Abdominal Aortic Aneurysm and Monitoring by 3D Ultrasound
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Published on: August 4, 2022

Hyperglycemia limits experimental aortic aneurysm progression.

Noriyuki Miyama1, Monica M Dua, Janice J Yeung

  • 1Division of Vascular Surgery, Stanford University School of Medicine, Stanford, Calif, USA.

Journal of Vascular Surgery
|August 4, 2010
PubMed
Summary

Hyperglycemia, or high blood sugar, was found to slow the growth of experimental abdominal aortic aneurysms (AAAs) in mice. Insulin therapy to lower blood sugar reduced this protective effect, suggesting new avenues for AAA treatment.

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Area of Science:

  • Vascular Biology
  • Metabolic Disease Research
  • Atherosclerosis and Aneurysm Studies

Background:

  • Diabetes mellitus (DM) is paradoxically associated with slower progression of abdominal aortic aneurysm (AAA) disease.
  • The underlying biological mechanisms for this observed negative correlation between DM and AAA progression remain largely unknown.
  • Understanding these mechanisms could reveal novel therapeutic targets for AAA.

Purpose of the Study:

  • To investigate the influence of elevated serum glucose concentrations on the progression of experimental AAA.
  • To elucidate the cellular and molecular mechanisms by which hyperglycemia affects AAA development.

Main Methods:

  • Abdominal aortic aneurysms were induced in hyperglycemic (DM) and normoglycemic mice using porcine pancreatic elastase (PPE) or angiotensin II (ANG) infusion.
  • Aneurysm progression was monitored via serial ultrasound; cellularity, proteolytic activity, and macrophage infiltration were assessed post-sacrifice.
  • The effect of hyperglycemia on macrophage migration was studied in a separate peritonitis model.

Main Results:

  • Hyperglycemic mice exhibited significantly reduced AAA enlargement compared to normoglycemic controls, irrespective of the induction method (PPE or ANG).
  • Reduced aortic mural macrophage infiltration, decreased elastolysis, and lower neovascularization were observed in hyperglycemic mice.
  • Insulin therapy in hyperglycemic mice partially reversed the protective effect, leading to intermediate AAA enlargement rates.

Conclusions:

  • Hyperglycemia demonstrably reduces the progression of experimental AAA disease in mouse models.
  • Lowering serum glucose levels with insulin therapy diminishes this inhibitory effect, indicating glucose's role.
  • Further research into the mechanisms of hyperglycemic aneurysm inhibition may yield new clinical strategies for AAA treatment.