Whole blood aggregation, coagulation, and markers of platelet activation in diet-induced diabetic C57BL/6J mice

Melissa Henry, Lisa Davidson, Zoe Cohen, Paul F. McDonagh, Paul E. Nolan, Leslie S. Ritter

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

Abstract

Aims: Type 2 diabetes in humans is associated with hypercoaguability; however, little is known about platelet function in mouse models of type 2 diabetes used to study this disorder. Therefore, the purpose of this study was to examine platelet aggregation, coagulation, and markers of platelet activation in a diet-induced mouse model of type 2 diabetes. Methods: Four week old, male, C57BL/6J mice were randomized to a standard chow or high fat (60% beef lard) diet for 4 months. To examine platelet function we measured ADP-induced whole blood aggregometry, whole blood coagulation by thromboelastography, tail bleeding times, platelet microparticle and platelet expression of p-selectin and platelet expression of CD61 by flow cytometry. Results: Diabetic mice exhibited less aggregation (p < 0.05), less coagulation (p < 0.01), prolonged tail bleeding times (n.s.), and lower agonist stimulated platelet CD61 expression (p < 0.001) compared to non-diabetic mice. There was no difference in platelet microparticle and platelet p-selectin expression. Conclusions: Diet-induced type 2 diabetic mouse do not demonstrate the hypercoagulability and platelet activation typically observed in humans with this disorder. More studies are warranted to further explore platelet function in this mouse model; to determine their applicability for studying these alterations in type 2 diabetes.

Original languageEnglish (US)
Pages (from-to)11-18
Number of pages8
JournalDiabetes Research and Clinical Practice
Volume84
Issue number1
DOIs
StatePublished - Apr 2009

Keywords

  • C57BL/6J mice
  • CD61
  • Diet-induced diabetes
  • Obesity
  • Platelets
  • Type 2 diabetes
  • p-selectin

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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