To determine the contribution of tissue protein reserves to lactational performance, multiparous female Sprague-Dawley rats were mated, caged individually and offered a diet high in protein (215 g crude protein (N x 6.25; CP)/kg dry matter (DM);H) ad lib. until day 12 of gestation. Subsequently half the rats continued to receive diet H while the remainder were offered a diet low in protein (65 g CP/kg D M ; L) until parturition. This treatment aimed to produce a difference in carcass protein at parturition. On day 1 of lactation females were allocated to either diet H or a low-protein diet (90 g CP/kg DM;L,) offered until day 13 of lactation, giving four lactation treatment groups HH, HL,, L H and LL,. Groups of females were slaughtered on days 2 and 12 of gestation and days 1 and 13 of lactation and carcass and major organs were analysed. Weight gain of standardized litters was used as an indicator of lactational performance. Maternal carcass protein contents at parturition were 43.5 (SE 1.2) and 38.7 (SE 0.8) g (P < 0.01) for diets H and L respectively. During lactation there was little change in carcass protein content of HH rats while L H rats appeared to replenish their depleted reserves. Food intake or lactational performance did not differ between these two groups. HL, and LL, rats lost carcass protein with HL, rats losing more than LL, rats (P < 0.05). Intake and lactational performance were reduced compared with that on diet H (P < 0.05) but for the first 6 d of lactation were both greater (P < 0.05) for diet HL, than for diet LL,. All four groups showed a considerable loss of body fat during lactation which was not affected by diet. The ability of HL, rats to catabolize more protein and consume more food allowed them to sustain a greater lactational performance. Previous maternal protein depletion had no influence on lactational performance as long as an adequate supply of dietary protein was provided.

The effects of severe protein restriction following parturition on the changes in rat milk composition during lactation were investigated using multiparous female Sprague-Dawley rats caged individually following mating and offered a high-protein diet (H; 215 g crude protein (N x 625; CP)/kg dry matter (DM)) ad lib. until parhition. Following parturition, half the females continued to receive diet H, whilst the remainder were offered a diet low in protein (L; 90 g CP/kg DM) ad lib. On days 2, 4, 8 and 12 of lactation groups of females from both dietary treatments were used to provide a milk sample. Milk samples were analysed for their lactose (enzymically), protein (binding to Coomassie blue), lipid (gravimetrically) and mineral (spectrophotometrically) contents. The milk lactose concentration of group H increased with stage of lactation (9 0.85, P < 0.001). Such an increase was prevented by diet L, and from day 8 of lactation the milk lactose of group L was lower (P < 0.05) than in group H. Group H milk protein concentration did not change during lactation and averaged 90.7 mg/g. Dietary protein restriction reduced the milk protein concentration of group L so that on days 2, 4 and 12 of lactation it was lower (P < 0-05) than that of group H. On day 8 of lactation the milk protein concentration of group L had increased (P < 0.05) and was comparable with that of group H. For group H, milk lipid averaged 166.8 mg/g and was generally unchanged during lactation. Diet L increased (P < 0.01) the milk lipid concentration (205-5 mg/g) compared with diet H and this was also significant on days 4 and 8 of lactation (P < 0.05). Group L milk lipid concentration also increased between days 4 and 8 of lactation (P < 0.05). Milk Na concentration declined during lactation in both dietary groups (P < 0.01) but was unaffected by dietary treatment. Both milk Ca and P concentrations increased (P < 0.01) during lactation in both dietary groups, whilst protein restriction also increased the Ca and P concentrations (P < 005). Milk K and Mg concentrations were unaffected by dietary treatment or stage of lactation. This significant alteration in the milk composition of severely protein-restricted dams, while possibly favouring the disposal of greater quantities of energy-yielding nutrients, suggests that equations developed for the estimation of milk production in rats cannot be used under such conditions. Lactation: Milk composition: Feed intake: Dietary protein: Rat Despite the fact that the laboratory rat has been used extensively as a model in nutritional and biochemical studies of lactation, and that numerous experiments have provided information on rat milk composition and the changes associated with lactation, the * For reprints. available at https://www.cambridge.org/core/terms. https://doi

The present study was undertaken to investigate the changes in muscle protein turnover involved in the rapid mobilization of protein in rats subjected to severe protein restriction during lactation. Estimates of mammary gland and liver protein synthesis were also made during lactation. Multiparous female Sprague-Dawley rats, caged individually following mating, were offered a high-protein diet (H; 215 g crude protein (N x 6-25; CP)/kg dry matter @M)) ad lib. until parturition. Following parturition, half the females continued to receive diet H, whilst the remainder were offered a diet low in protein (L; 90 g CP/kg DM) ad lib. On days 2, 4, 8 and 12 of lactation, groups of females were used in the estimation of tissue protein synthesis (flooding dose of [3H]phenylalanine) immediately after a milk sample had been obtained. Rates of muscle protein synthesis were unchanged during lactation in group H. The feeding of diet L during lactation reduced the muscle protein synthesis on day 12 to rates that were lower than group H and also the rate on diet L on day 2 (P < 0.01). However, this fall in muscle protein synthesis was not rapid and muscle fractional synthesis rate (FSR) was different from group H only from day 8 (P c 0.05).Estimated rates of mammary protein synthesis appeared to be generally unchanged by dietary treatment or stage of lactation. Liver FSR was also unchanged by dietary protein supply or stage of lactation. The effect of dietary protein restriction on liver size and protein content during lactation influenced liver absolute synthesis rate (ASR), and on days 8 and 12 of lactation liver ASR was lower in group L than in group H (P < 0.001). The loss of muscle protein in rats fed on diet L during lactation (133 mg) occurred mainly between days 2 and 8 of lactation and was primarily associated with a dramatic increase in degradation (13.0% per d), with the decline in synthesis having a much smaller role. A decline in muscle protein degradation during the latter half of lactation was part of the mechanism that prevented excessive muscle protein catabolism. It is thought that the estimation of mammary protein synthesis in the present study was impaired by the milk sampling procedure previously used.

Changes in tissue protein synthesis and an associated membrane transport system in rats were investigated during lactation and under conditions of dietary protein restriction. Following mating, female Sprague-Dawley rats (second parity) were caged individually and offered a high-protein diet (H; 215 g crude protein (N x 625; CP)/kg dry matter (DM)) ad lib. until day 12 of gestation. Subsequently half continued to receive diet H, whilst the remainder were offered a low-protein diet (L; 65 g CP/kg DM) until parturition. On day 1 of lactation females were then allocated to either diet H or another lowprotein diet (L,; 90 g CP/kg DM) which were offered ad lib. until day 13 of lactation, giving four lactation groups HH, LH, HL, and LL,. On days 1 and 13 of lactation groups of females were used in the estimation of tissue protein synthesis (flooding dose of [3H] phenylalanine) and NaC, K+-ATPase (EC 3.6.1.3) activity @olarographically) in skeletal muscle, mammary gland, liver and duodenal mucosa. By day 1 of lactation diet L had reduced fractional and absolute synthesis rates (FSR and ASR) of muscle protein (P c 0.05) and the 0, consumption associated with Na+,K+-ATPase, although not significantly (P < 0.10). Rates of protein synthesis in the other tissues studied were not affected on day 1 of lactation by the gestation dietary treatment. By day 13 of lactation the feeding of diet L, had reduced muscle FSR and ASR of group HL, to rates that were lower than those on day 1 (P < O-M), comparable to those of group LL, and lower than those of groups HH and LH (P < 0.05). Diet H had allowed group LH to increase their muscle protein synthesis compared with that on day 1 (P < 0.05). Muscle Na+,K+-ATPase activity on day 13 of lactation was also lower in groups offered diet L, (P < 0.05). Mammary protein synthesis was increased during lactation with the feeding of diet H (P < 0.05), which was prevented by diet L, such that rates of groups HL, and LL, were lower than those of the two high-protein groups on day 13 (P c 001). Mammary respiration and in particular Na+,K+-ATPase activity was increased during lactation by the feeding of diet H (P < 0.05). Rates of protein synthesis and respiration in liver and duodenal mucosa were not significantly affected by the gestational or lactational dietary treatments. Calculated rates of muscle protein degradation suggest that whilst the loss of muscle protein in group HL, during lactation might have been promoted by the decline in synthesis, the increase in degradation may have been quantitatively more important.Lactation: Protein synthesis : Na+,K+-ATPase: Rat When dietary protein is limiting, the extent of maternal protein reserve repletion at parturition has a significant impact on a female's ability to sustain lactation, with more * For reprints. In our earlier studies we did not make any measurements of tissue protein metabolism. A purpose of the work reported here was to explore the influence of feeding protein in gestation and in lactation on rates of protein synthesis in differen...