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Action of Enterally Administered Ornithine α‐Ketoglutarate on Protein Breakdown in Skeletal Muscle and Liver of the Burned Rat

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Several studies concerning burn patients have shown that supplementation of enteral nutrition with ornithine α‐ketoglutarate (OKG) favorably modifies protein metabolism. Therefore, the effect of OKG administration on muscular and hepatic protein catabolism was evaluated in burned rats. Four groups of six rats were used. Two groups were scalded by immersion of the dorsum in water at 90°C for 10 seconds and then starved for 24 hours. Controlled enteral nutrition was then administered in three boluses daily (Osmolite, 210 kcal/kg/d, 1.2 g N/kg/d); one group was supplemented with OKG (5 g/ kg/d, ie, 0.68 g N/kg/d), while the other group received an equivalent amount of nitrogen in the form of glycine. One group of healthy control rats received Osmolite supplemented with glycine and the last group was fed ad libitum. The animals were killed after 2 days of nutrition. Protein catabolism was assessed in vitro by measuring the amount of valine (liver catabolism) and phenylalanine (muscle catabolism) released into the incubation medium of isolated tissues. Tissular and serum glutamine were also assayed. Burn injury induced muscle hypercatabolism without affecting hepatic catabolism. The administration of OKG limited both muscle weight loss and muscle protein hypercatabolism and significantly improved the muscle glutamine pool. These results demonstrate the nitrogen‐sparing effect of OKG in muscle in hypercatabolic states. (Journal of Parenteral and Enteral Nutrition 15:517–520, 1991)
Title: Action of Enterally Administered Ornithine α‐Ketoglutarate on Protein Breakdown in Skeletal Muscle and Liver of the Burned Rat
Description:
Several studies concerning burn patients have shown that supplementation of enteral nutrition with ornithine α‐ketoglutarate (OKG) favorably modifies protein metabolism.
Therefore, the effect of OKG administration on muscular and hepatic protein catabolism was evaluated in burned rats.
Four groups of six rats were used.
Two groups were scalded by immersion of the dorsum in water at 90°C for 10 seconds and then starved for 24 hours.
Controlled enteral nutrition was then administered in three boluses daily (Osmolite, 210 kcal/kg/d, 1.
2 g N/kg/d); one group was supplemented with OKG (5 g/ kg/d, ie, 0.
68 g N/kg/d), while the other group received an equivalent amount of nitrogen in the form of glycine.
One group of healthy control rats received Osmolite supplemented with glycine and the last group was fed ad libitum.
The animals were killed after 2 days of nutrition.
Protein catabolism was assessed in vitro by measuring the amount of valine (liver catabolism) and phenylalanine (muscle catabolism) released into the incubation medium of isolated tissues.
Tissular and serum glutamine were also assayed.
Burn injury induced muscle hypercatabolism without affecting hepatic catabolism.
The administration of OKG limited both muscle weight loss and muscle protein hypercatabolism and significantly improved the muscle glutamine pool.
These results demonstrate the nitrogen‐sparing effect of OKG in muscle in hypercatabolic states.
(Journal of Parenteral and Enteral Nutrition 15:517–520, 1991).

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