(3) and (4) (P < 0-05 and P = 0-073, respectively). In turn, villous height was significantly correlated (r = 0-78 to 0-87, P < 0-05) with the rate of bodyweight gain after weaning in these two groups. For piglets offered ewes' milk plus glutamine, an increase in DM intake was associated only with increases in crypt depth (P < 0-01). These data show that the structure and function of the small intestine can be preserved when a milk diet is given after weaning, and suggest an association between food intake and villous height in determining post-weaning weight gain. were offered ewes' fresh milk every 2 h in a feeding schedule that increased from 1-2 I per piglet on the 1st day after weaning to 2-4 I on days 4 and 5. On the 5th day all piglets were killed and samples of small intestine were taken for histological and biochemical examination. Feeding ewes' milk or ewes' milk plus 20 g L-glutamine per I maintained (P > 0-05) villous height and crypt depth compared with piglets killed at weaning. In contrast, piglets given a dry starter diet had shorter villi (P < 0-001), deeper crypts (P < 0-001), and proportionately 0-21 to 0-28 less protein (P>0-05) in their intestinal mucosa. Piglets given the starter diet proportionately grew from 0-49 to 0-62 more slowly (P < 0-01), ate the same amount of dry matter (DM; P > 0-05), but consumed proportionately 0-30 less energy (P < 0-001) than their counterparts given the milk diets. No treatment differences in the specific activity of lactase and sucrase were observed (P>0-05). Significant correlations existed between voluntary food intake and villous height at the proximal jejunum for piglets given the starter diet and ewes' milk

This study was designed to test the degree of protein loss that may be sustained by lactating sows before milk biosynthesis and ovarian function will be impaired. First-parity Camborough x Canabrid sows were allocated to receive isocaloric diets (61 +/- 2.0 MJ of ME/d) and one of three levels of protein intake in lactation: 1) 878 g of CP and 50 g of lysine/d (n = 8), 2) 647 g of CP and 35 g of lysine/d (n = 7), or 3) 491 g of CP and 24 g of lysine/d (n = 10). Every 5 d during a 23-d lactation, sow live weight, backfat depth, and litter weight were recorded, and a preprandial blood sample was collected. Milk samples were collected on d 10 and 20 of lactation. Sows were slaughtered on the day of weaning, and liver and ovarian variables were measured. Lower dietary protein intakes elicited progressively larger live weight losses during lactation (-13, -17, and -28 +/- 2.3 kg; P < 0.001), but similar and minimal backfat losses (-1.3 +/- 0.29 mm). Approximately 7, 9, and 16% of the calculated body protein mass at parturition was mobilized by d 23. Lactation performance did not differ among treatments until d 20, at which time approximately 5, 6, and 12% of the calculated protein mass at parturition had been lost. The milk protein concentration on d 20 of lactation reflected the amount of body protein lost, and was lowest (P < 0.05) in sows that lost the most protein. After d 20, piglet growth rate decreased (P < 0.05) in a manner related to the amount of body protein lost. At weaning, ovarian function was suppressed in sows that had mobilized the most body protein; they had fewer medium-sized follicles (> 4 mm; P < 0.05), their follicles contained less (P < 0.01) follicular fluid, and had lower estradiol (P < 0.05) and IGF-I (P < 0.10) contents. Culture media containing 10% pooled follicular fluid (vol/vol) from high-protein-loss sows were less able to support nuclear and cytoplasmic maturation of oocytes in vitro, evidenced by more oocytes arrested at metaphase I (P < 0.05) and showing limited cumulus cell expansion (P < 0.06). Plasma insulin and IGF-I concentrations did not seem to be related to the observed differences in animal performance. Our data suggest that no decline in lactational performance or ovarian function when a sow loses approximately 9 to 12% of its parturition protein mass. However, progressively larger decreases in animal performance are associated with a loss of larger amounts of body protein mass at parturition.

Effects of differential patterns of feed intake during lactation, associated metabolic and endocrine changes, and reproductive status after weaning were investigated in 26 primiparous sows suckled by six piglets. Sows were fed to appetite (Group AA; n = 9) from d 1 to 28 of lactation or restricted to 50% from d 22 to 28 (Group AR; n = 9) or from d 1 to 21 (Group RA; n = 8). Sow weight, backfat, and litter weights were recorded weekly. After weaning sows were tested twice daily for onset of estrus and inseminated twice using pooled semen. At d 28 of gestation sows were slaughtered and reproductive tracts were recovered to determine ovulation rate and embryo number. Intensive blood sampling was carried out for 12-h periods on d 21 and before and after weaning on d 28 to characterize changes in plasma LH, FSH, insulin, and IGF-I by RIA. Litter growth rates did not differ among groups. Feedrestricted sows lost more (P < .01) body weight and backfat than those fed to appetite. During periods of feed restriction in AR and RA sows, postprandial insulin, mean IGF-I, and LH pulse frequency were less than in AA sows fed to appetite. All sows exhibited an increase (P < .001) in LH pulsatility in response to weaning. After weaning, no differences were observed in insulin, LH, or FSH, although IGF-I was still lower (P < .05) in AR sows. Weaning-toestrus interval increased in AR and RA sows and ovulation rate was lower (P < .05) than in AA sows. Embryo survival did not differ between RA and AA sows but was lower (P < .01) in AR sows. These results demonstrate that the pattern of metabolic change in the primiparous lactating sow exerts differential effects on fertility after weaning.

not available

The hypothesis tested in this experiment was that the structure and function of the small intestine of piglets given a milk liquid diet after weaning depends on their level of energy intake. At weaning (28 days)

The effect of the timing of nutritional changes during the immediate period after mating on early embryonal survival and of progesterone as a potential mediator of such changes was studied. A total of 82 gilts were initially fed 2.5 kg.gilt-1.d-1 for one estrous cycle before they were inseminated at 16 and 24 h after the onset of estrus (d 0) using fresh, pooled semen. After AI, gilts were randomly allocated to one of the three feeding regimens, normal NRC allowance of 1.5 x maintenance per day from d 1 (Group N1) or d 3 (Group N3) or an allowance of 2 x maintenance from d 1 (Group H1). All gilts were fed on an individual basis. Single blood samples were collected 72 h after first detection of standing estrus. From d 15 onward, all gilts were fed 1.8 kg/d until they were slaughtered on d 28 +/- 3. Total and viable empryonal survival were affected by dietary treatment (P = .044 and .027, respectively), and viable embryonal survival in group N1 was greater than in group H1 (84.7 +/- 4.5 vs 64.5 +/- 7.6%; P < .05). Plasma progesterone was greater in group N1 than in groups N3 and H1 (10.5 +/- 1.0 vs 3.7 +/- .8 and 4.5 +/- .7 ng/mL, respectively; P < .05). The timing of the change in feed allowance after mating is therefore crucial for demonstrating effects of nutrition on embryonal survival in gilts, and progesterone may mediate these effects.

It is possible that pathogenesis of or susccotibility to joint abnormality differs among animals studied, even in the same experiment, resulting in a failure to observe a correIation between a certain factor and the occurrence of leg abnormalities. The last part

We investigated the effect of body protein mass at parturition and different degrees of body protein loss in lactation on sow performance. In a 2 x 2 factorial arrangement, 77 Genex gilts were fed to achieve either a standard or high body mass at parturition and to lose either a moderate (MPL) or high (HPL) amount of protein in lactation. Pregnant gilts were fed either 24.4 MJ of ME, 266 g of CP, and 11 g of lysine/d or 34.0 MJ of ME, 436 g of CP, and 20 g of lysine/d resulting in divergent (P < 0.01) live weights (165 vs. 193 kg) and calculated protein masses (24.3 vs. 30.0 kg) and slightly different backfat depths (20.0 vs. 22.8 mm; P < 0.05) at parturition. Diets fed during lactation were formulated to deliver 731 g of CP and 37 g of lysine/d or 416 g of CP and 22 g of lysine/d to induce differential body protein mobilization. Sows were slaughtered at weaning (d 26), and the weight of the organs and the lean, fat, and bone in five primal cuts was measured. The external diameter of the eight largest follicles on each ovary was recorded, and the follicular fluid from these follicles was collected, weighed, and analyzed for estradiol. Losses in lactational live weight (26 vs. 20 kg; P < 0.01) and calculated protein mass (17.8 vs. 10.7%; P < 0.001) were greater, and the carcass lean mass at weaning was 10% lighter (P < 0.05) in HPL sows. Backfat (5.1 +/- 0.8 mm; P = 0.29) and calculated fat mass (25.8 +/- 1.5%; P = 0.84) losses did not differ between treatments. Both sow body mass (P < 0.05) and lactation protein loss (P < 0.01) affected litter growth rate. Litter growth rate decreased (P < 0.05) at the end of lactation in HPL sows once these sows had lost 10 to 12% of their calculated protein mass. Ovarian follicular development was most advanced in high body mass sows that lost the least protein; these sows had the heaviest (P < 0.05) uterine weight and highest (P < 0.05) follicular fluid estradiol concentration. Follicular development was least advanced in standard body mass sows that lost the most protein. These sows had the lowest (P < 0.05) muscle:bone ratio at weaning and likely lost the largest proportion of their muscle mass compared with the other treatments. In conclusion, ovarian function at weaning and litter performance was higher in high body mass sows and in sows that lost the least protein in lactation, suggesting that a larger lean mass may delay the onset of a decrease in performance in sows that lose protein in lactation.