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Related Experiment Video

Updated: May 24, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Hyperinsulinemia does not change atherosclerosis development in apolipoprotein E null mice.

Christian Rask-Madsen1, Erica Buonomo, Qian Li

  • 1Research Division, Joslin Diabetes Center, Boston, MA, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|March 20, 2012
PubMed
Summary

Hyperinsulinemia, or high insulin levels, does not accelerate atherosclerosis development in mice lacking the apolipoprotein E gene. This suggests insulin resistance, not just high insulin, is key for atherosclerosis progression.

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Related Experiment Videos

Last Updated: May 24, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

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Published on: September 26, 2018

Quantification of Atherosclerosis in Mice
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Quantification of Atherosclerosis in Mice

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Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
06:43

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus

Published on: December 7, 2013

Area of Science:

  • Cardiovascular Research
  • Metabolic Syndrome
  • Atherosclerosis Pathogenesis

Background:

  • Hyperinsulinemia is linked to metabolic syndrome and cardiovascular disease.
  • The direct role of hyperinsulinemia in atherosclerosis development remains unclear.
  • Insulin resistance is a known contributor to atherosclerosis.

Purpose of the Study:

  • To investigate the causal role of hyperinsulinemia in atherosclerosis development.
  • To determine if elevated insulin levels accelerate atherosclerosis in the absence of significant insulin resistance.
  • To elucidate the contribution of impaired insulin clearance to hyperinsulinemia and atherosclerosis.

Main Methods:

  • Utilized apolipoprotein E (Apoe) null mice with targeted insulin receptor (Insr) gene knockout.
  • Compared Insr haploinsufficient/Apoe null mice with Apoe null littermates.
  • Assessed plasma insulin, glucose tolerance, insulin sensitivity, insulin signaling, and atherosclerotic lesion development.

Main Results:

  • Insr haploinsufficient/Apoe null mice exhibited significant hyperinsulinemia due to impaired insulin clearance.
  • No differences were observed in glucose tolerance, insulin sensitivity, plasma lipids, or blood pressure between groups.
  • Atherosclerotic lesion size and cholesterol abundance were similar in both groups up to 52 weeks.

Conclusions:

  • Hyperinsulinemia alone, without significant insulin resistance or altered lipids/blood pressure, does not promote atherosclerosis.
  • Impaired insulin clearance is a primary driver of hyperinsulinemia in this model.
  • These findings highlight the importance of insulin resistance in the link between metabolic dysfunction and cardiovascular disease.