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Leukocyte endogenous mediator alters protein dynamics in rats


, : Leukocyte endogenous mediator alters protein dynamics in rats. Metabolism Clinical & Experimental 32(7): 654-660

Leukocyte endogenous mediator (LEM), a low MW peptide synthesized by monocytic cells during phagocytosis, was implicated as the host's initiator of the protein metabolic response to infection and inflammation. To determine whether administration of LEM would alter protein kinetics, appearance and oxidation of plasma tyrosine as well as the rates of protein synthesis in liver and skeletal muscle were determined in fasted rats that received a 30-h continuous infusion of either physiologic saline, LEM, or heat-inactivated LEM. The LEM was obtained from rabbit peritoneal exudate and the treatment solutions supplied 2.8 .times. 108 cell equivalents/100 g of body weight (BW) per day. Endogenous tyrosine oxidation increased from 4.0 .+-. 0.4 .mu.mol/100 g BW per h to 5.4 .+-. 0.7 .mu.mol/100 g BW/h in animals infused with heat-inactivated LEM and to 7.5 .+-. 1.5 .mu.mol/100 g BW/h in rats receiving LEM (P < 0.01). Nonsecretory protein synthesis in the liver was greatest in rats administered LEM (2239 .+-. 325 mg/d) when compared with control groups receiving physiologic saline (1122 .+-. 195 mg/d) or heat-inactivated LEM (1374 .+-. 62 mg/d; P < 0.01), whereas skeletal protein synthetic rates were unchanged. Rates of muscle and collagen protein breakdown were estimated from the urinary excretion rate of Nt-methylhistidine and hydroxyproline, respectively, and their excretion rose by 30% (P < 0.05) and 42% (P < 0.05) with LEM administration. Administration of LEM apparently stimulates a mobilization of amino acids from peripheral tissues to support increased visceral protein anabolism while whole body amino acid oxidation is also enhanced. Since similar effects follow fever and infection, these results suggest that LEM may play an underlying role in the protein metabolic response to infection and inflammation.

US$19.90

PMID: 6865755

DOI: 10.1016/0026-0495(83)90120-8


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