Corticosterone accelerates atherosclerosis in the apolipoprotein E-deficient mouse

Mitsuharu Okutsu*, Vitor A. Lira, Kazuhiko Higashida, Jonathan Peake, Mitsuru Higuchi, Katsuhiko Suzuki

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)


Chronic stress is an important risk factor for atherosclerosis, which is a chief process in the development of cardiovascular disease. Increased circulating levels of corticosterone have been documented in several animal models of chronic stress. However, it remains to be established whether corticosterone is sufficient to exacerbate atherosclerosis. To test this hypothesis, apolipoprotein E (ApoE)-deficient mice were fed a high-fat diet for 13 weeks with exposure to either corticosterone or vehicle in the drinking water (CORT and Con). Corticosterone treatment significantly increased atherosclerotic plaque area at the aortic root. Such exacerbation of atherosclerosis was accompanied by significantly lower levels of circulating white blood cells and serum interleukin-1β (IL-1β), and significantly elevated serum concentrations of total cholesterol, low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL) and small dense low-density lipoprotein (sd-LDL) in CORT mice when compared to Con mice. These findings demonstrate that corticosterone is sufficient to exacerbate atherosclerosis invivo despite its anti-inflammatory properties and that this marked pro-atherogenic phenotype is primarily associated with increased dyslipidaemia.

Original languageEnglish
Pages (from-to)414-419
Number of pages6
Issue number2
Publication statusPublished - 2014 Feb


  • ApoE-deficient mice
  • Cholesterol
  • Dyslipidaemia
  • Hypothalamic-pituitary-adrenal axis
  • Stress

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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