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Preparation of Washed Human Platelets for Quantitative Metabolic Flux Studies
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Advanced glycation end products strongly activate platelets.

Thomas Gawlowski1, Bernd Stratmann, Ruth Ruetter

  • 1Heart and Diabetes Center NRW, Ruhr-University Bochum, Georgstrasse 11, 32545, Bad Oeynhausen, Germany. tgawlowski@hdz-nrw.de

European Journal of Nutrition
|July 28, 2009
PubMed
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Advanced glycation end products (AGEs) acutely activate platelets, increasing surface markers and the receptor for AGEs (RAGE). This suggests a mechanism where dietary AGEs may contribute to postprandial ischemic events in conditions like diabetes.

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Area of Science:

  • Biochemistry
  • Hematology
  • Endocrinology

Background:

  • Diabetes mellitus is linked to hyperglycemia, a key factor in diabetic complications like cardiovascular disease.
  • Hyperglycemia elevates advanced glycation end products (AGEs), which are implicated in disease pathogenesis.
  • Platelet activation is a known contributor to the development of cardiovascular diseases.

Purpose of the Study:

  • To investigate whether advanced glycation end products (AGEs) acutely induce platelet activation.
  • To determine if exogenous AGEs trigger a response in platelets.

Main Methods:

  • Purified food- and serum-derived AGEs were incubated with isolated human platelets in vitro.
  • Platelet activation was assessed by measuring surface markers CD62 and CD63 via flow cytometry.
  • Receptor for AGEs (RAGE) expression on platelet membranes was also quantified using flow cytometry.

Main Results:

  • Both food- and serum-derived AGEs significantly increased CD62 and CD63 expression on platelets.
  • Increased expression of CD62 and CD63 was dependent on AGE concentration and incubation time.
  • Incubation with AGEs or thrombin led to a twofold increase in RAGE expression on platelet surfaces.

Conclusions:

  • Elevated surface activation markers and RAGE expression on platelets were observed at AGE concentrations found in vivo after consuming food or drinks.
  • These findings suggest signaling pathways for dietary AGEs that may promote acute postprandial ischemic events.
  • The study highlights a potential link between dietary AGEs, platelet activation, and cardiovascular risk.