Effect of inflammatory and noninflammatory stress on plasma ketone bodies and free fatty acids and on glucagon and insulin in peripheral and portal blood.
Inflammatory stress as characterized by infection with Streptococcus pneumoniae, administration of endotoxin, or the induction of a turpentine abscess is characterized by the inhibition of the ketosis assoicated with fasting and a decline in the level of free fatty acids in the plasma. Moreover, rats subjectd 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 noninflammatroy stresses did not show an abnormal elevation of plasma or portal insulin or glucagon.
D000818:Animals; D001769:Blood; D005230:Fatty Acids, Nonesterified / Q000097:blood*; D005934:Glucagon / Q000097:blood*; D007249:Inflammation / Q000097:blood*; D007328:Insulin / Q000097:blood*; D007657:Ketone Bodies / Q000097:blood*; D008297:Male; D011168:Portal System; D051381:Rats; D012149:Restraint, Physical; D013217:Starvation / Q000097:blood; D013312:Stress, Physiological / Q000097:blood
D005230:Fatty Acids, Nonesterified; D007328:Insulin; D007657:Ketone Bodies; D005934:Glucagon