A 2 X 2 factorial arrangement with two levels (0, 660 ppm) of vitamin C and two levels (0, 55 ppm) of carbadox supplementation was used in two experiments with 112 crossbred pigs weaned between 4 and 5 wk of age. An 18% protein corn-soybean meal-oats-dried whey starter diet was used as the basal diet. Each diet was fed ad libitum for a 4-wk period to three replicates of four pigs in Exp. 1 and to four replicates of four pigs in Exp. 2. Vitamin C supplementation produced a significantly higher plasma vitamin C concentration in weanling pigs, but, contrary to results of our previous study, failed to improve average daily gain of the pigs. Daily gain was, however, improved significantly by carbadox supplementation. Carbadox also produced a significantly higher plasma vitamin C concentration in pigs after a 7-d lag period. Plasma Fe concentration of pigs was not affected by supplemental vitamin C, but was significantly higher in those fed carbadox-supplemented diets. Plasma ceruloplasmin concentration increased significantly in all treatment groups from the initial sampling period (d 0) to subsequent periods. No interactions between supplemental vitamin C and carbadox were observed in daily gain, feed efficiency and the measured plasma constituents.

Cement kiln dust (CKD) samples of which have been reported to stimulate growth in cattle and sheep, was fed to weanling pigs in a 42-d experiment. CKD at levels of 1.5 and 3.0% was added to a corn-soybean meal-oats-whey-type diet containing inadequate amounts of Ca (.4% of the diet) to provide final dietary Ca levels of .85 and 1.3%. A diet containing 3% limestone (1.3% dietary Ca) served as a positive control. Body weight gain was depressed by 3.0% CKD, and histopathological lesions of the humerus, not typical of nutritional secondary hyperparathyroidism or rickets, were observed. The lesions detected were osteonecrosis, thinning of the cortex and reduction in the width of the epiphyseal cartilage. Width of the proximal epiphyseal plate and cortical index of the humerus (width of cortex divided by total diameter at narrowest point of diaphysis) were smaller in pigs fed 3% CKD than in pigs fed 3% limestone. CKD contained 2.3% A1, 15 ppm Cd and 110 ppm Pb, providing 690, .45 and 3.3 ppm of A1, Cd and Pb, respectively, in the diet containing 3% CKD. Kidney, liver and bone ash concentrations of these three minerals were not increased by CKD, and typical toxicity signs were absent. It is concluded that CKD may contain one or more factors that interfere with normal bone metabolism in growing pigs when the diet contains 3.0% CKD.

A 2 X 2 factorial arrangement with two genotypes of pigs (genetically obese and lean) and two dietary treatments (basal, a 16% protein corn-soybean meal standard grower diet, and basal +220 ppm thyroprotein as iodinated casein) was used. The 28 gilts were housed individually and fed ad libitum from 121 d of age until slaughtered at 99 kg body weight. Compared with lean pigs, genetically obese pigs had significantly lower average daily gain and gain/feed, greater backfat thickness, smaller loin eye area, shorter carcass length and lower circulating plasma triiodothyronine (T3) concentration. However, both total plasma and free thyroxine (T4) concentrations were similar comparing obese and lean pigs. Supplementation with thyroprotein increased circulating plasma concentration of both total and free T4 and produced interactions with genotype in affecting daily gain and gain/feed of pigs. Thyroprotein reduced both daily gain and gain/feed in obese pigs, but increased daily gain and gain/feed in lean pigs. It is suggested, similar to the case with obese mice, that heat production of our genetically obese pigs may be more sensitive to thyroprotein administration compared with similar treatment of lean animals.

Nineteen Landrace sows mated to Landrace boars were randomly assigned, on d 91 of pregnancy, to three groups: (1) control (six sows)--fed standard 13% protein corn-soybean meal gestation diet at 1.82 kg/d to d 112 of pregnancy; (2) 4-d fast (seven sows)--fed standard gestation diet to d 94 of pregnancy, fasted from d 95 to 98 of pregnancy and then refed a semipurified fat-free diet ad libitum until d 112 of pregnancy, and (3) 8-d fast (six sows)--treated the same as groups 2, except that the fast began on d 91 and extended through d 98 of pregnancy. The fat-free diet consisted of dextrose and soybean meal and was fortified with minerals and vitamins. On d 112 of pregnancy, all fetuses were removed by Caesarean section and determinations were made of fetal body and liver weights, fetal liver and gastrocnemius muscle glycogen concentrations, and maternal uterus and peritoneal adipose tissue glycogen levels. Sows in groups 2 and 3 consumed more (P less than .01) average daily feed during the refeeding period than did the control sows. Fasting and refeeding failed to affect maternal or fetal tissue glycogen concentration, or fetal body or liver weight. Average sow tissue glycogen concentrations were .23 and 3.0 mg/g tissue for peritoneal adipose tissue and uterus, respectively. Average fetal liver and gastrocnemius muscle glycogen concentrations were, 87 and 62 mg/g tissue, respectively. Average fetal body and liver weights were 1,287 and 39.5 g/fetus, respectively. We conclude that fasting followed by refeeding of a fat-free diet to pregnant sows during late gestation does not increase maternal or fetal tissue glycogen content and appears to be of no value in enhancing pig survival in early postnatal life.