Energy substrate metabolism in fresh and stored human platelets

Phin Cohen; Benjamin Wittels

doi:10.1172/JCI106210

^{Department of Biochemistry, the State University of Utrecht, The Netherlands}

^{Department of Medicine, Harvard Medical School and the Peter Bent Brigham Hospital, Boston, Massachusetts 02115}

^{Department of Pathology, Duke University Medical School, Durham, North Carolina 27706}

Find articles by Cohen, P. in: JCI | PubMed | Google Scholar

^{Department of Biochemistry, the State University of Utrecht, The Netherlands}

^{Department of Medicine, Harvard Medical School and the Peter Bent Brigham Hospital, Boston, Massachusetts 02115}

^{Department of Pathology, Duke University Medical School, Durham, North Carolina 27706}

Find articles by Wittels, B. in: JCI | PubMed | Google Scholar

Published in Volume 49, Issue 1 on January 1, 1970
J Clin Invest. 1970;49(1):119–127. https://doi.org/10.1172/JCI106210.
© 1970 The American Society for Clinical Investigation

Published January 1, 1970 - Version history

The latent capacity of human platelets for oxidizing several important energy-yielding substrates has been revealed by hypoosmolaric incubation conditions.

The data show that the human platelet has a considerable capacity to oxidize both glucose and long-chain fatty acids. Long-chain fatty acids appear to rank favorably with glucose as a potential energy substrate. In a number of mammalian tissues, (—)-carnitine serves to regulate the rate at which long-chain fatty acids are oxidized. Evidence was obtained which suggests that (—)-carnitine functions in a similar role in the platelet.

After storage of human platelets at 4°C for 24 hr, the oxidative capacity for glucose was reduced by approximately 25% and for long-chain fatty acids by almost 50%. Investigation of the component parts of the metabolic pathways indicated that a marked decrease in the capacity of the Krebs cycle could be responsible for the decrement in energy substrate oxidation.

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