A probable endocrine basis for the depression of ketone bodies during infectious or inflammatory state in rats.
The effects of infection with Streptococcus pneumoniae, Francisella tularensis, and Venezuelan equine encephalitis virus as well as inflammatory stress induced by the administration of turpentine and endotoxin on plasma ketone bodies and insulin were studied in white rats. All of the infectious/inflammatory stresses caused a significant decrease in the ketonemia of fasting and an elevation of plasma insulin. When a pneumococcal infection was initiated in a diabetic rat, inhibition of fasting ketonemia did not occur. Similarly, pneumococcal infection in the hypophysectomized rat did not result in a noticeable depression of either fasting ketonemia or plasma FFA. The increase in circulating insulin appears to be closely correlated with the inhibition of fasting ketonemia noted in the infectious/inflammatory stress.
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000097:blood; D004671:Encephalitis, Arbovirus / Q000097:blood*; D004731:Endotoxins; D004926:Escherichia coli; D005260:Female; D007016:Hypophysectomy; D007249:Inflammation / Q000097:blood*; D007657:Ketone Bodies / Q000097:blood*; D008070:Lipopolysaccharides; D008297:Male; D011008:Pneumococcal Infections / Q000097:blood*; D051381:Rats; D014406:Tularemia / Q000097:blood*; D014425:Turpentine
D004731:Endotoxins; D007657:Ketone Bodies; D008070:Lipopolysaccharides; D014425:Turpentine