Modification of glucocorticoid-induced changes in myofibrillar protein turnover in rats by protein and energy deficiency as assessed by urinary excretion of Ntau-methylhistidine.
The effects of differing degrees of experimental protein-energy malnutrition on the response of myofibrillar protein turnover rates to administration of corticosteroid has been studied in two experiments on rats. The basal control diet, offered ad lib. in each case, contained 40 g protein/kg, and other groups received diets containing 62 X 5, 95 or 220 g protein/kg at 0 X 67, 1 or 1 X 5 times the level of the control energy intake. Daily administration of 25 or 30 mg corticosterone/kg body-weight after 18 d pre-feeding caused an increase in plasma protein, glucose and insulin concentrations, but a decrease in the corticosterone: insulin values. Liver size and protein content increased, as did the fractional excretion of dietary nitrogen as urea-N in all treated groups. However, whereas a fall in food intake and body-weight occurred in one experiment the reverse occurred in the other. Ntau -Methylhistidine excretion was 12% lower for rats receiving 40 v. 220 g protein/kg diet and excretion was increased by only 57 v. 90% respectively, when the two groups of rats were given 30 mg corticosterone/kg per d. Rats which received 25 mg corticosterone/kg per d and up to 95 g protein/kg diet increased excretion of Ntau -methylhistidine by an average 35%. The fractional degradation rate of myofibrillar protein (kd) was reduced by about 10% by the low-protein diet from 3 X 1 to 2 X 8%/d. During corticosterone treatment the increment in kd for rats on this diet was only 60% of that for rats receiving the 220 g protein/kg diet, i.e. an increase of 1 X 8 v. 3 X 0%/d. Energy restriction further reduced kd during low-protein intake but did not affect the response to the corticosterone. Variations in dietary protein from 40 to 95 g/kg had little effect on the increase in kd during steroid treatment. The effect of corticosterone on calculated synthesis rates (ks) differed markedly between experiments. While ks fell by 50-65% in rats which lost weight on treatment, it rose by up to 60% in rats where carcass non-collagen-protein accretion remained unchanged or increased, despite an increase in kd. Protein deficiency decreases the catabolic response to glucocorticoid, but the net metabolic response appears crucially dependent on changes in food intake or the stage of growth of the rat or both. A net anabolic response with increased fractional rates of myofibrillar protein breakdown, synthesis and accretion was observed in growing rats fed on relatively-low-protein diets and given 25 mg corticosterone/kg per d.(ABSTRACT TRUNCATED AT 400 WORDS)
D000818:Animals; D001823:Body Composition / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D003345:Corticosterone / Q000494:pharmacology*; D004032:Diet; D004044:Dietary Proteins / Q000378:metabolism*; D002149:Energy Intake / Q000187:drug effects; D008099:Liver / Q000378:metabolism; D008297:Male; D008762:Methylhistidines / Q000652:urine; D009210:Myofibrils / Q000187:drug effects / Q000378:metabolism*; D009584:Nitrogen / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D011502:Protein-Energy Malnutrition / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D004044:Dietary Proteins; D008762:Methylhistidines; D009584:Nitrogen; D003345:Corticosterone