Depression of glucose utilization by Intralipid in the post-traumatic period: an experimental study.
We investigated the accelerated clearance of Intralipid (IL) in the immediate post-traumatic period and the influence of the concomitant rise in fatty acid ((FFA) metabolism on carbohydrate tolerance. As a result we postulate that intermediary products of fatty acid oxidation inhibit key enzymes in the glycolytic pathway. The fatty acidemia and its metabolic sequlae can be avoided by intermittent Intralipid supplementation (at low rates) during TPN. It will assure (1) a larger carbohydrate-to-fat caloric ratio during infusion and (2) cyclical regeneration of the enzyme systems involved in lipid metabolism.
D000818:Animals; D000941:Antigens; D001786:Blood Glucose / Q000378:metabolism; D002914:Chylomicrons / Q000097:blood; D003864:Depression, Chemical; D004195:Disease Models, Animal; D004285:Dogs; D004837:Epinephrine / Q000097:blood; D005217:Fat Emulsions, Intravenous / Q000378:metabolism*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005934:Glucagon / Q000097:blood / Q000276:immunology; D005947:Glucose / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism; D009638:Norepinephrine / Q000097:blood; D013997:Time Factors; D014947:Wounds and Injuries / Q000378:metabolism*
D000941:Antigens; D001786:Blood Glucose; D002914:Chylomicrons; D005217:Fat Emulsions, Intravenous; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D005934:Glucagon; D005947:Glucose; D009638:Norepinephrine; D004837:Epinephrine