Related Experiment Video
Updated: Jul 15, 2026

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
Published on: November 16, 2011
Impaired Glucose Tolerance is Associated with Enhanced Platelet-Monocyte Aggregation in Short-Term High-Fat Diet-Fed
Zibusiso Mkandla1, Tinashe Mutize1, Phiwayinkosi V Dludla2,3
1School of Laboratory Medicine and Medical Sciences (SLMMS), College of Health Sciences, University of KwaZulu-Natal, Durban 4000, South Africa.
Abstract:
High-fat diet (HFD) feeding is known to induce metabolic dysregulation, however, less is known on its impact in promoting the hypercoagulable state. This current study aimed to evaluate platelet-monocyte aggregate (PMA) formation following short-term HFD feeding. This is particularly important for understanding the link between inflammation and the hypercoagulable state during the early onset of metabolic dysregulation. To explore such a hypothesis, mice were fed a HFD for 8 weeks, with body weights as well as insulin and blood glucose levels monitored on a weekly basis during this period. Basal hematological measurements were determined and the levels of spontaneous peripheral blood PMAs were assessed using whole blood flow cytometry. The results showed that although there were no significant differences in body weights, mice on HFD displayed impaired glucose tolerance and markedly raised insulin levels. These metabolic abnormalities were accompanied by elevated baseline PMA levels as an indication of hypercoagulation. Importantly, it was evident that baseline levels of monocytes, measured using the CD14 monocyte marker, were significantly decreased in HFD-fed mice when compared to controls. In summary, the current evidence shows that in addition to causing glucose intolerance, such as that identified in a prediabetic state, HFD-feeding can promote undesirable hypercoagulation, the major consequence implicated in the development of cardiovascular complications.
Insights
High-fat diet (HFD) feeding promotes hypercoagulation by increasing platelet-monocyte aggregates (PMA). This early metabolic dysregulation links inflammation to cardiovascular risks.
Area of Science:
- Metabolic research
- Hematology
- Cardiovascular science
Background:
- High-fat diet (HFD) is known to cause metabolic dysregulation.
- The impact of HFD on inducing a hypercoagulable state is not well understood.
- Understanding the link between inflammation and hypercoagulation in early metabolic dysfunction is crucial.
Purpose of the Study:
- To investigate the effect of short-term HFD feeding on platelet-monocyte aggregate (PMA) formation.
- To assess the relationship between HFD-induced metabolic changes and hypercoagulation.
- To determine if HFD promotes a hypercoagulable state.
Main Methods:
- Mice were fed a HFD for 8 weeks.
- Body weights, insulin, and blood glucose levels were monitored weekly.
- Basal hematological measurements and spontaneous peripheral blood PMA levels were assessed using whole blood flow cytometry.
Main Results:
- HFD feeding resulted in impaired glucose tolerance and elevated insulin levels, despite no significant body weight changes.
- Baseline PMA levels were significantly elevated in HFD-fed mice, indicating hypercoagulation.
- Baseline monocyte levels (CD14 marker) were significantly decreased in HFD-fed mice.
Conclusions:
- Short-term HFD feeding induces glucose intolerance, characteristic of a prediabetic state.
- HFD feeding promotes hypercoagulation, evidenced by increased PMAs.
- This hypercoagulable state is a significant factor in the development of cardiovascular complications.

