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Effect of inflammatory and noninflammatory stress on plasma ketone bodies and free fatty acids and on glucagon and insulin in peripheral and portal blood

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Abstract

Inflammatory stress as characterized by infection withStreptococcus pneumoniae, administration of endotoxin, or the induction of a turpentine abscess is characterized by the inhibition of the ketosis associated with fasting and a decline in the level of free fatty acids in the plasma. Moreover, rats subjected to these inflammatory stresses demonstrate a significant rise in peripheral and portal insulin and glucagon. Rats subjected to noninflammatory stresses, screen-restraint, or noninvasive femoral fracture did not demonstrate the inhibition of ketosis but did show a decrease in plasma free fatty acids. The noninflammatory stresses did not show an abnormal elevation of plasma or portal insulin or glucagon.

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Authors and Affiliations

  1. United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, 21701, Frederick, Maryland

    Mitchell V. Kaminski Jr., Harold A. Neufeld & Judith G. Pace

  2. St. Mary of Nazareth Hospital Center, 60622, Chicago, Illinois

    Mitchell V. Kaminski Jr., Harold A. Neufeld & Judith G. Pace

Authors
  1. Mitchell V. Kaminski Jr.
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  2. Harold A. Neufeld
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  3. Judith G. Pace
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The views of the authors do not purport to reflect the positions of the Department of the Army or the Department of Defense.

In conducting the research described in this report, the investigators adhered to the “Guide for the Care and Use of Laboratory Animals,” as promulgated by the Committee on the Revision of the Guide for Laboratory Animal Facilities and Care of the Institute of Laboratory Animal Resources, National Research Council. The facilities are fully accredited by the American Association for Accreditation of Laboratory Animal Care.

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Kaminski, M.V., Neufeld, H.A. & Pace, J.G. Effect of inflammatory and noninflammatory stress on plasma ketone bodies and free fatty acids and on glucagon and insulin in peripheral and portal blood. Inflammation 3, 289–294 (1979). https://doi.org/10.1007/BF00914186

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  • DOI: https://doi.org/10.1007/BF00914186

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