Skip to main content

Diabetes mellitus

Diabetes mellitus

Grant:
  • Cardiovascular Elite Postdoctoral Grant
Organ System:
  • Cardiovascular
Date Funded:
  • 23 March, 2020
Chief Investigator/s:
  • Dr. Tessa Barrett

Project summary

Assessing diabetes mellitus platelet hyperactivity to provide insight into the mechanisms by which they contribute to unresolved inflammation.

What is the issue for NSW?

In Australia, 6% of adults have diabetes mellitus (DM), which is associated with a doubled risk of heart attack, precipitated by atherosclerotic cardiovascular disease. In the past 25 years, the prevalence of DM in Australia has more than tripled and projected to rise.

An estimated one-third of young adults will develop DM during their lifetime, translating to increased risk of cardiovascular (CV) events.

Despite the high CVD burden associated with DM, the pathways responsible for elevated risk are incompletely understood. CV risk factors often seen in conjunction with DM include hyperglycaemia, atherogenic dyslipidemia, insulin resistance and low-grade systemic inflammation – all of which may contribute to platelet and myeloid hyperactivity. Platelet hyperactivity is independently associated with long-term mortality and CV events. Notably platelets from DM subjects are more hyperreactive and less responsive to current antiplatelet, antithrombotic-based therapies.

What does the research aim to do and how?

Dr Barrett has recently found that platelets primarily associate with macrophages in atherogenesis, the inflammatory hallmark of lesions, and directly mediate myeloid inflammatory responses accelerating atherogenesis [12, 13]. Moreover, Dr Barrett has found myeloid cells and platelets to be hyper-inflammatory in DM indicating these interactions are exacerbated in DM.

Dr Barrett’s research proposes that an unbiased approach to assess DM platelet hyperactivity will provide insight into the mechanisms by which they contribute to unresolved inflammation, an increasingly appreciated risk factor for CVD. Additionally, this approach is likely to facilitate the development of a new class of therapeutics to suppress platelet inflammatory potential (i.e. distinct from therapies that curtail their thrombotic actions, aspirin and; P2Y12 inhibitors) translating to reduced platelet-mediated inflammation in CVD, especially in those with DM.