Human C-reactive protein induces endothelial dysfunction in biobreeding diabetic rats

Ishwarlal Jialal, Harmeet Kaur, Sridevi Devaraj, Gerred Smith

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


Objective: C-reactive protein (CRP) levels in diabetes predict cardiovascular events. Also, human CRP (hCRP) exacerbated the proinflammatory, pro-oxidant and procoagulant states in a spontaneous model of type 1 diabetes mellitus (T1DM), the biobreeding (BB) rat. Since there is a paucity of data examining the role of CRP on endothelial dysfunction in animal models of diabetes, we tested this hypothesis in the diabetic BB rat. Methods: Diabetic BB rats (n = 4 per group) were injected with human serum albumin (HSA) or hCRP [hCRP = 20 mg/ kg body weight; intraperitoneal (IP)] for three consecutive days. The rats were euthanized on day 4. Biomarkers that were assayed included endothelin-1 (ET-1), soluble intracellular adhesion molecule-1 (sICAM-1), Von Willebrand factor (vWF) and 6-keto prostaglandin F1-alpha (6-keto PGF1-α) in plasma. Results: hCRP administration resulted in a significant increase in plasma levels. Furthermore, hCRP-treated rats had significantly increased circulating levels of ET-1 (1.12 ± 0.6 pg/mL versus 0.4 ± 0.21 pg/mL), vWF (45 ± 2.4 ng/mL versus 34 ± 7 ng/mL) and sICAM-1 (41 ± 3 ng/mL versus 34 ± 3.4 ng/mL) compared to HSA-treated rats (p < 0.05). There was no significant effect on 6-keto PGF1-α levels. Conclusion: Hence, in this preliminary report, we make the novel observation that hCRP induces endothelial dysfunction in a spontaneous model of T1DM, and this could have implications for the vascular complications in diabetics.

Original languageEnglish (US)
Pages (from-to)550-553
Number of pages4
JournalDiabetes and Vascular Disease Research
Issue number6
StatePublished - Nov 2013


  • C-reactive protein
  • endothelial dysfunction
  • inflammation
  • type 1 diabetes mellitus

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Internal Medicine
  • Cardiology and Cardiovascular Medicine


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