The influence of ketosis on the metabolic response to skeletal trauma.
Intravenous glucose and ketone body feeding were compared for their potential in altering urinary nitrogen losses by the traumatized rat. Eighteen male rats were traumatized by bilateral femoral fracture. The rats were fed totally by vein for 3 days prior and 3 days after injury and the infusion rate was held constant over the 6 days of infusion. Group GT rats were fed glucose as the source of nonprotein energy while group MT rats were fed a mixture of 72% monoacetoacetin (the monoglyceride of acetoacetate)-28% glucose for the nonprotein energy. Total urinary nitrogen excretion on a 24-hr basis was measured for each of the 6 days of intravenous feeding. On the third day post-trauma, each rat was evaluated for leucine kinetics using a continuous infusion of L-[1-14C]leucine and measurement of breath and plasma specific activities. Rats from group MT were hyperketonemic and normoglycemic and rats from group GT were normoketonemic and hyperglycemic. Urinary nitrogen losses, leucine oxidation, and leucine turnover were similar for the two groups. We conclude that ketone bodies are as good an intravenous source of energy as is glucose, and the ketone bodies do not cause hyperglycemia.
D000090:Acetoacetates / Q000378:metabolism; D000138:Acidosis / Q000378:metabolism*; D000818:Animals; D001835:Body Weight; D003300:Copper / Q000652:urine; D005264:Femoral Fractures / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D005989:Glycerides / Q000378:metabolism; D006943:Hyperglycemia / Q000209:etiology; D007657:Ketone Bodies / Q000378:metabolism*; D007662:Ketosis / Q000378:metabolism*; D007930:Leucine / Q000493:pharmacokinetics; D008297:Male; D009584:Nitrogen / Q000652:urine; D010288:Parenteral Nutrition; D051381:Rats; D011919:Rats, Inbred Strains; D015032:Zinc / Q000652:urine
D000090:Acetoacetates; D005989:Glycerides; D007657:Ketone Bodies; C020417:monoacetoacetin; D003300:Copper; D007930:Leucine; D005947:Glucose; D015032:Zinc; D009584:Nitrogen