The effect of long-term dietary protein excess and deficit on whole-body protein-N turnover (WBPNT) was examined in lambs nourished by intragastric infusions of nutrients. Ten sheep were given 500 mg N/kg metabolic weight m75) per d from casein for 2 weeks and then either 50 (L), 500 (M) or 1500 (H) mg N/kgWo.75 per d for 6 weeks. Volatile fatty acids were infused at 500 kJ/kgWo" per d. Daily WBPNT was measured by continuous intravenous infusion of [l-'3C]leucine 3 d before, and on days 2,21 and 42 after the alteration in protein intake. Whole-body protein-N synthesis (WBPNS) was calculated as the difference between WBPNT and the protein-N losses as urinary NH3 and urea. Wholebody protein-N degradation (WBPND) was then estimated from WBPNS minus protein gain determined from N balance. Fractional rates of WBPNS and WBPND were calculated against fleece-free body N content. WBPNS rates at the L, M and H intakes were respectively 35.1,41.5 amd 63.7 g/d (P < 0.001) on average over the 6 weeks and WBPND rates were 39.5,41-1 and 568 g/d (P < 0.001). The fractional rates of WBPNS were 5.01, 6.37 and 7.73% per d (P < 0.001) while those of WBPND were 5.64, 6.29 and 6.81 % per d (P < 0-005) respectively. On days 2,21 and 42, WBPNS rates at intake H were 54.0, 61-8 and 75.4 g/d (P = 0-03) respectively, and WBPND rates were 43.2,564 and 70.9 g/d (P = 0.03); at intake L the amounts were 38.2, 34.2 and 32.8 g/d for WBPNS (P = 0,003) and for WBPND were 43-4, 38.0 and 36.9 g/d (P = 0.016) respectively. There were no significant (P > 0.05) differences in

The relationships of N input or protein status and the concentrations of serum insulin-like growth factor-1 (IGF-1), plasma fibronectin (FN) and total protein (TP) were examined in three experiments with steers and sheep nourished by intragastric infusion of nutrients. In Expt 1, three steers (340 kg live weight) were infused with three levels of volatile fatty acids (0,300 and 600 kJ/kg metabolic weight (w0'75) per d) and six levels of casein (0, 200, 400, 650, 1500 and 2500 mg N/kg W0'75 per d). Each N treatment was imposed for 5 d. In Expts 2 and 3, five groups of sheep (about 35 kg live weight) were infused with casein at 500 mg N/kg vv0.75 per d for 2 weeks followed by 1500,500 or 50 mg N/kg W0'75 per d in Expt 2, and in Expt 3, with 100 mg N/kg w0 75 per d for 6 weeks or 10 mg N/kg W0'75 per d for 4 weeks. Non-protein energy was maintained constant at 500 kJ/kg w0'75 per d throughout. Daily N balance and total body N content at the end were measured, and protein status was defined as a percentage of cumulative N accretion or depletion in relation to the total body N content at maintenance. It was found that IGF-1 and FN responded rapidly and substantially to altered N input, and that when daily N input was maintained constantly at sub-maintenance, their continuous declines were related closely to progressive protein depletion in the sheep. Plasma TP concentration was independent of N input when N input was altered acutely in the steers, but declined significantly and gradually with severe, chronic body protein depletion in the sheep. Plasma content of TP in the sheep however reduced acutely with a reduction in N input. Plasma volume fell substantially over the first 2 weeks of protein depletion, compensating for the declines in TP content and maintaining TP concentration plateau. The possible implications of the changes in TP concentration and content (concentration x volume) to body protein loss in sheep are discussed. IGF-1: Fibronectin: Protein status: RuminantsThe estimation of changes in total body N can be achieved using some advanced noninvasive laboratory techniques such as neutron activation analysis, tracer dilution methods and some instrument techniques (reviewed by Gibson, 1990 andEllis, 1992). However these techniques cannot easily be applied in practical situations. Several blood biochemical metabolites have therefore been studied as potential indicators of protein status in human subjects and animals (see reviews by Gibson, 1990;Young et al. 1990 central role in the regulation of whole-body protein metabolism by reconstituting absorbed and degraded tissue amino acids, removing N in the body by production of urea, using amino acids in gluconeogenesis, influencing protein synthesis via production of its insulinlike growth factor-1 (IGF-1) and producing and exporting plasma proteins to transport nutrients. It may, therefore, be possible to use the metabolic products which reflect liver function as an indicator of whole-body protein status. Plasma IGF-1 (Baxter, 1986) 1989). The present study ...