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Nutrients, such as dietary lipids, can influence development of the central nervous system [1, 2]. Particularly, an increase in plasma concentrations of cholesterol, which is an essential constituent of all animal cells (especially of brain) and abundant in milk, is positively associated with enhancement of cerebrum weight gain and behavioral development [2–4]. Additionally, docosahexaenoic acid (DHA) is a component of complex lipid in membranes, nerve insulation, as well as a precursor for signaling molecules (including prostaglandins). The availability of long-chain polyunsaturated fatty acids, including DHA, also modulates eicosanoid metabolism and myelination during growth spurt of the brain [5,6]. Interestingly, dietary DHA supply enhances visual and neurological development both in prematurely born infants [7] and in term infants [8,9], while promoting problem-solving and childhood intelligence [10]. The beneficial influences of dietary cholesterol and DHA on brain development are currently interpreted as modification of the membrane structure and functions of membrane-associated proteins [11]. Nitric oxide (NO), synthesized from L-arginine by NO synthase (NOS), plays an important role in development and function of the brain [12]. All isoforms of the NOS [neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS)] are present in neurological tissue. Of particular interest, nNOS activity is decreased when the protein is phosphorylated at the inhibition site of Ser 852, whereas eNOS activity is increased when the enzyme is phosphorylated at the activation site of Ser 1177 [12]. GTP-CH activity, Tetrahydrobiopterin (BH4), which is synthesized from GTP via the GTP cyclohydrolase I (GTP-CH) pathway [13], is an essential cofactor of NOS [14]. NO is a potent signal that regulates many physiological processes affecting behavior and cognitive function, including synaptic plasticity during long term potentiation and depression [15]. NO also acts as a retrograde messenger to stabilize or refine synapse during development, as a regulatory second messenger involved in the control of brain blood flow, and as an agent that contributes to both brain degeneration and neuropotection [16]. Additionally, NO promotes angiogenesis, redox state, cell immunity, and neuronal survival [14,17]. Cholesterol and DHA are known to regulate NO synthesis in vascular endothelial cells [17]. We hypothesized that dietary supplementation with cholesterol and DHA can influence the arginine-NO pathway in the brain of neonatal animals. This hypothesis was tested with piglets by measuring NOS activity, total and phosphorylated levels for the three NOS isoforms, as well as concentrations of arginine, BH4 and NADPH in brain. To determine whether the effects of DHA and cholesterol are specific to the neuronal tissue, we also analyzed the above parameters in skeletal muscle and liver.

Cholesterol and docosahexaenoic acid (DHA) are important nutrients for neural development of infants. However, little is known about the effect of cholesterol or DHA on concentrations of amino acids (AA) in neonatal tissues. This study was conducted with the piglet (an established model for studying human infant nutrition) to test the hypothesis that dietary supplementation with the lipids may modulate AA availability in tissues. Sixteen newborn pigs were nursed by sows for 24 h and then assigned to one of four treatment groups, representing supplementation with 0.0% (control), 0.2% cholesterol, 0.2% DHA, or cholesterol plus DHA to the basal milk-formula. All piglets were euthanized at 49 days of age. In brain, cholesterol supplementation reduced (P < 0.05) concentrations of glutamate, serine, glutamine, threonine, β-alanine, alanine, methionine, isoleucine, leucine, and γ-aminobutyrate but increased (P < 0.05) concentrations of glycine and lysine, whereas DHA supplementation similarly affected (P < 0.05) concentrations of the same AA (except for isoleucine and lysine) and taurine. In addition, concentrations of most AA in liver, muscle and plasma were substantially altered by dietary supplementation of cholesterol and DHA in a tissue-dependent manner. Further, DHA reduced concentrations of carnosine in skeletal muscle, as well as ammonia in both plasma and brain. The results reveal that cholesterol and DHA can regulate AA metabolism and availability in various tissues of piglets. These novel findings have important implications for designing the next generation of infant formula to optimize neonatal growth and development.

Little is known about the mechanism responsible for retarded placental and fetal growth induced by maternal dietary protein malnutrition. On the basis of the recent finding that nitric oxide (NO) and polyamines (products of L-arginine) play an important role in embryonic and placental development, the present study was designed to determine whether protein deficiency decreases placental and endometrial activities of NO synthase (NOS) and ornithine decarboxylase (ODC) (the first and key regulatory enzyme in polyamine synthesis). Primiparous gilts selected genetically for low or high plasma total cholesterol concentrations (low line and high line, respectively) were mated and then fed 1.8 kg/d of isocaloric diets containing 13% or 0.5% crude protein. At d 40 or 60 of gestation, they were hysterectomized, and placenta and endometrium were obtained for incubations, NOS and ODC assays, and measurements of free amino acids and polyamines. Maternal dietary protein restriction decreased arginine and ornithine concentrations, constitutive and inducible NOS activities and NO production, as well as ODC activity and polyamine concentrations in placenta and endometrium of both lines of gilts. Placental NO synthase activity and NO generation were lower in high line gilts than in low line gilts. ODC activities and polyamine concentrations in placenta and endometrium were decreased at d 60 compared with d 40 of gestation. These changes in placental and endometrial synthesis of NO and polyamines during early gestation may be a mechanism responsible for reduced placental and fetal growth in protein-deficient gilts and for altered conceptus development in high line gilts.

Sixty-eight female neonatal pigs selected for seven (Experiment 1) or eight (Experiment 2) generations for high (HG) or low (LG) plasma cholesterol were used to test the hypothesis that neonatal dietary cholesterol fed during the first 4 or 8 wk of postnatal life increases the cholesterol content of the cerebrum in young adulthood following free access to a high-fat (15%), high-cholesterol (0.5%) diet from 8 to 20 or 24 wk of age. Pigs were removed from their dams at 1 d of age and given free access to a sow-milk replacer diet containing 9.5% coconut fat and 0 or 0.5 % cholesterol. All pigs (except four HG and four LG pigs in Experiment 2, which were deprived of cholesterol throughout the study) were fed the high-fat, high-cholesterol diet from 8 wk to termination at 20 or 24 wk of age. Cerebrum weight and cholesterol concentration were higher in pigs fed cholesterol neonatally than in those deprived of cholesterol neonatally in both experiments, but weight and cholesterol concentration were unaffected by genetic line. Cholesterol concentrations in longissimus and semitendinosus muscles and in subcutaneous fat were unaffected by diet or genetic line. We conclude that dietary cholesterol deprivation during the first 4 to 8 wk of life in piglets is associated with lower cholesterol concentration and total content in the young adult cerebrum than in pigs supplemented with cholesterol in early life. These data support previous observations and suggest the possibility of a metabolic need for neonatal dietary cholesterol in normal brain development.

To test the hypothesis that maternal protein deprivation in early pregnancy retards body and organ growth of 63-d (midterm) pig fetuses, 16 primiparous domestic four-way crossbred swine were fed a diet adequate in protein (13% protein) (A) or a protein-restricted (0.7% protein) diet (PR) from d 1 to 63 of pregnancy or to parturition. Maternal body weight, plasma protein, hematocrit, and heart and spleen weights were reduced, and indices of body fatness were increased by the PR diet. Fetal body weights were reduced and fetal placental weights were increased at d 63 by protein restriction. Length from crown to rump and weights of liver, kidney, gastrointestinal tract, and cerebrum were lower in PR than in A fetuses. Concentrations of protein, RNA and DNA in liver, cerebrum and longissimus muscle were unaffected by maternal diet, but total amounts of all three constituents in liver and cerebrum were lower in PR than in A. Relative organ weights were similar in A and PR fetuses except that kidneys and gastrointestinal tract were greater in A fetuses. Newborn body weights and absolute organ weights were generally lower in PR than in A, but relative weights were similar. The observed reduction in body and organ weights and amounts of protein, RNA and DNA in 63-d fetuses and newborn progeny of PR swine establishes that the stunting effect of maternal protein restriction can be initiated by midterm, preceding the period of most rapid accretion of body tissues during prenatal life in the pig.

Thirty-two castrated male crossbred growing pigs (average initial wt 26.9 kg) were used to determine the effect of a high level of dietary protein (37%) compared with a normal level of protein (15%) on enterobacteria and Campylobacter sp. inhabitation in the large intestine and on visceral organ hypertrophy and the interrelationships between these two factors. Pigs were kept in pairs (eight pens of two pigs/diet) and fed their respective diets and libitum. Eight pigs (two pens of two pigs fed each diet) were killed at wk 4, 8, 12 and 16 without fasting. Fecal samples were obtained every 2 wk from animals scheduled for necropsy at 16 wk, and colon contents were obtained from all pigs at necropsy; samples were enumerated individually for enterobacteria and Campylobacter sp. Weights of heart, lungs, liver, kidneys, perirenal fat and empty stomach, small intestine and large intestine were recorded at necropsy. Stomach, cecum and proximal colon were sectioned for histopathologic examination. Daily body weight gain was depressed by high dietary protein, but liver and kidneys were heavier in the high protein group than in controls at each time interval. Mild lymphoid hyperplasia of Peyer's patches in the small intestine in some pigs in both groups was indicative of antigenic stimulation but not of pathologic significance. There was no effect of diet on counts of enterobacteria or Campylobacter sp. in feces or colon contents during the 16-wk experiment. We conclude that the hypertrophic response of the tissues of growing pigs to high dietary protein is not the result of the presence of Campylobacter sp. or enterobacteria in the colon contents.

High iron consumption has been proposed to relate to an increase in the risk of colon cancer, whereas high levels of supplemental sodium phytate effectively reduce iron-induced oxidative injury and reverse iron-dependent augmentation of colorectal tumorigenesis. However, the protective role of intrinsic dietary phytate has not been determined. In this study, we examined the impact of removing phytate present in a corn-soy diet by supplemental microbial phytase on susceptibility of pigs to the oxidative stress caused by a moderately high dietary iron intake. Thirty-two weanling pigs were fed the corn-soy diets containing two levels of iron (as ferrous sulfate, 80 or 750 mg/kg diet) and microbial phytase (as Natuphos, BASF, Mt. Olive, NJ, 0 or 1200 units/kg). Pigs fed the phytase-supplemented diets did not receive any inorganic phosphorus to ensure adequate degradation of phytate. After 4 months of feeding, liver, colon, and colon mucosal scrapings were collected from four pigs in each of the four dietary groups. Colonic lipid peroxidation, measured as thiobarbituric acid reacting substances (TBARS), was increased by both the high iron (P< 0.0008) and phytase (P< 0.04) supplementation. Both TBARS and F2-isoprostanes, an in vivo marker of lipid peroxidation, in colonic mucosa were affected by dietary levels of iron (P< 0.03). Mean hepatic TBARS in pigs fed the phytase-supplemented, high iron diet was 43%-65% higher than that of other groups although the differences were nonsignificant. Moderately high dietary iron induced hepatic glutathione peroxidase activity (P= 0.06) and protein expression, but decreased catalase (P< 0.05) in the colonic mucosa. In conclusion, intrinsic phytate in corn and soy was protective against lipid peroxidation in the colon associated with a moderately high level of dietary iron.

Twenty-eight genetically obese and 24 lean barrows (65.0 and 68.7 kg average BW, respectively) were allotted within genotype to a 16% CP corn-soybean meal basal diet or this basal diet + 20 ppm ractopamine (a phenethanolamine beta-adrenergic agonist) and allowed ad libitum access to feed for 48 d. Compared to lean pigs, obese pigs had lower ADG, gain to feed ratio, longissimus muscle area, predicted amount of muscle, and weights of trimmed loin and ham, ham lean, heart, spleen, kidney and gastrointestinal tract (P less than .05). Obese pigs also had shorter carcass but higher dressing percentage, backfat thickness, fat depth, fat area, untrimmed loin weight and fasting plasma urea N concentration (P less than .05). Dietary supplementation with 20 ppm ractopamine reduced daily feed intake and improved gain to feed ratio in both lean and obese pigs (P less than .05). Pigs fed ractopamine had shorter carcasses, less fat depth and fat area, smaller weights of stomach and colon plus rectum, but higher dressing percentages, longissimus muscle areas, weights of trimmed Boston butts, picnics and loins, ham lean and predicted amounts of muscle than pigs not fed ractopamine (P less than .05). Supplemental ractopamine had no effect on fasting plasma concentrations of urea N, nonesterified fatty acids, triglyceride or glucose (P greater than .05). No genotype x ractopamine interactions for the criteria described above were detected (P greater than .05). These results suggest that ractopamine will improve the efficiency of feed utilization and carcass leanness in swine with different propensities for body fat deposition.

Seventy-two castrated male four-way composite (Chester White x Landrace x Large White x Yorkshire) weanling pigs (17 kg initial BW) were used to determine the compensatory response of specific organs and whole body following a 3-wk period of restricted energy intake imposed by ad libitum-feeding an 80% alfalfa meal diet or pair-feeding an adequate corn-soybean meal diet to attain equal weight loss. Six pigs were killed at d 0 to provide baseline data. Six pigs from each diet group (control, C; alfalfa, A, restricted, R) were killed at d 21, after which all remaining pigs were fed C ad libitum to 35 d, 105 d or 126 d. Six pigs per group were killed at 35 and 105 d and four per group were killed at 126 d. Organ weight and carcass data were recorded for all pigs at all time intervals. Regression of organ and trimmed lean tissue weights on time was tested for linearity (d 1 to 126 for C and d 21 to 126 for A and R except d 35 to 126 for gastrointestinal tract traits for A and R); differences in organ weights between C, A and R at d 21 and d 35 were tested by a two-way analysis of variance. There was no evidence of a compensatory growth response to dietary energy restriction for 21 d except for rate of change in weights of liver and kidneys and backfat depth from 21 to 126 d and of gastrointestinal tract components from 21 to 35 d. Specific organs may exhibit compensatory growth over different time spans in young pigs in the absence of observable weight compensation at the whole-animal level.

Thirty-six four-way cross (Chester White X Landrace X Large White X Yorkshire) growing barrows and gilts were used to investigate the effects of replacing graded levels of protein from soybean meal with equivalent levels of protein from rubber seed meal in 16% CP semipurified diets on the performance characteristics, hematocrit, plasma metabolites and N utilization of pigs. The first diet (control) was largely cornstarch-soybean meal in which the soybean meal supplied all of the CP. In other diets, rubber seed meal replaced 10%, 20% and 30%, respectively, of the protein of soybean meal in the control diet. Twenty gilts were used in a 28-d growth trial and 16 barrows were used in an 8-d digestion trial (4-d collection). There were no differences (P greater than .05) in ADG, ADF intake and in the feed:gain ratios, even though there was a trend for lower ADG and gain:feed ratio as the level of rubber seed meal increased in the diet. There were no differences in hematocrit, but plasma protein and albumin tended to be depressed when rubber seed meal provided more than 10% of the dietary protein. Apparent digestibilities of GE, DM and N were lower with rubber seed meal at 20% of the protein than with any other diet, but apparent N retained and the percent of digested N retained were not depressed significantly (P greater than .05). Although rubber seed meal protein is of poorer quality than soybean meal protein for growing pigs, at least 10% of dietary protein can be provided by rubber seed meal without adversely affecting growth and N utilization.

Three experiments were conducted with 96 growing Landrace × Yorkshire × Duroc crossbreds to determine the collective effectiveness of cereal phytase from wheat middlings, microbial phytase, and citric acid in improving phytate-P bioavailability in corn-soy diets. In Exp. 1, 40 gilts (7 wk old) were fed five diets for 8 wk. Diets 1, 2, and 3 were low-P, corn-soybean meal diets (CSB) + 0,.1, or.2% inorganic P (P i ) as calcium phosphate, respectively. Diet 4 was a similar corn-soy diet that included 15% wheat middlings (461 cereal phytase U/kg). Diet 5 was the CSB + microbial phytase (1,200 U/kg; Natuphos, BASF, Mount Olive, NJ). In Exp. 2, 16 barrows (8 wk old) were fed two diets for 6 wk. Diet 1 was the same as Diet 3 of Exp. 1 (.2% P i ). Diet 2 was Diet 4 of Exp. 1 + microbial phytase (300 U/kg). In Exp. 3, 40 barrows and gilts (6 wk old) were fed four diets for 6 wk. Diets 1 and 2 were the same as those in Exp. 2. Diet 3 was Diet 2 of Exp. 2 + 1.5% citric acid. Diet 4 was similar to Diet 3 but contained 10 instead of 15% wheat middlings. In Exp. 1, pigs fed the low-P, CSB (Diet 1) had lower (P

Twenty-four genetically obese and 24 lean barrows were allotted within genotype to either a 16% CP corn-soybean meal basal diet, the basal + .69 ppm cimaterol or the basal + 1.38 ppm cimaterol. Pigs had ad libitum access to their diets from 59.3 kg to 104.5 kg body weight. No genotype x cimaterol interactions were detected (P greater than .05). Neither genotype nor cimaterol supplementation had any effect (P greater than .05) on average daily weight gain or gain-to-feed ratio. Compared with lean pigs, obese pigs had higher fasting plasma urea nitrogen (BUN), a smaller gastrointestinal tract and a greater dressing percentage with a shorter and fatter carcass (P less than .05). Cimaterol produced a higher fasting plasma BUN, a greater dressing percentage with a leaner carcass and a higher shear force value for loin chops (P less than .05). Cimaterol also tended (P less than .10) to increase heart weight. However, no difference was observed in these measurements between pigs fed .69 or 1.38 ppm cimaterol. In lean pigs fed the basal or .69 ppm cimaterol diet, there was no difference (P greater than .05) in the 8 to 24 h postprandial whole-animal heat production. Cimaterol effectively decreased fat deposition and increased lean accretion both in genetically obese and in lean pigs; there were no differential responses to cimaterol in pigs with different propensities to deposit body fat.

Aquatic weeds from Cayuga Lake in New York were included as 10% or 20% dry weight of rations which were fed to growing pigs for 69 days. The animals gained weight at a rate comparable to those on a basal diet or a diet in which an equivalent weight of alfalfa replaced the aquatic plants. The feed efficiency (kg ration consumed/kg wt gained) of the aquatic rations was significantly lower, probably because of the lower nutritive value of the aquatic plants. Polychlorinated biphenyls (PCBs) were found in the aquatic plants (0.59 ppm, dry weight) and in the pig fat of those fed the aquatic ration. Hepatic microsomal mixed function oxidase activity was not significantly different in the animals fed the various treatment rations. Histopathologic examination of animal tissues revealed no lesions or abnormalities which could be attributed to the diets.

The effects of feeding restricted energy or restricted protein on blood constituents were studied in pregnant gilts. Gilts fed the protein-restricted diet through out gestation had lower hemoglobin, serum protein and serum albumin levels from week 10 to parturition, indicating depletion of labile protein reserves of the protein-restricted gilts to satisfy fetal requirements. The protein-restricted gilts (PR) developed edema between the hindlegs and around the vulva probably due to the low serum protein and albumin concentrations. There were no significant differences among groups in blood glucose and plasma FFA and all groups showed a significant rise in blood glucose after week 10. A reduced sensitivity to insulin occurring during pregnancy could account for this significant increase in glucose. Birth weight was significantly lower in PR group compared to control (C) and energy-restricted (ER) groups. It appears that changes in blood glucose and plasma FFA are not sensitive indices of energy needs in energy- or protein-restricted pregnant gilts and that only dietary protein deprivation affects blood hemoglobin, urea nitrogen, serum protein and albumin concentrations. J. Nutr. 104: 1033-1040, 1974.

Genetically obese (O) or lean (L) primiparous gilts were assigned on the day of mating to an adequate [control (C) or restricted (R)] intake of feed. Body weight and ultrasonically estimated backfat depth were recorded at wk 0 (mating), 4, 8, 12 and 16 of pregnancy, and at d 2-3, 21 and 28 of lactation. Number of pigs born, survival rate to 28 d of age and piglet body weight at 0, 14, 21 and 28 d of age were recorded. Four male and four female progeny from each diet group of each genetic strain were slaughtered at 6 mo of age for carcass and organ weight measurements. OR and LR gilts responded similarly to feed restriction in body weight change, backfat depth and plasma traits. Body weight increased throughout gestation in OC and LC gilts but decreased about 6 kg in OR and LR gilts. Backfat remained relatively constant throughout gestation in OC and LC gilts but declined steadily in LR and OR gilts. There were no genetic group x diet interactions for any trait measured. Litter size and piglet survival were not affected by diet or genetic group, but piglet birth weight and daily gain to d 28 and to wk 25 were lower in both R groups. Backfat accretion and other indices of carcass fatness were reduced in progeny of R dams.(ABSTRACT TRUNCATED AT 250 WORDS)

Thirty-two genetically lean and obese Yorkshire X Duroc crossbred castrated male pigs were divided within genetic line into two groups at 7 weeks of age. Eight pigs within each line were fed a diet low in fat and cholesterol (maize-soybean meal diet fortified with minerals and vitamins). The other group was fed a similar diet containing added beef tallow (11%) and dried egg yolk (1%). All pigs were fed ad libitum for 4 months when one-half of each group was slaughtered. All other pigs were continued on their respective diets at a restricted level of intake for an additional 5 months at which time the protein source of two pigs in each diet group within each genetic line was changed from soybean meal to casein. After an additional 6 months on their respective diets (16 months total duration of experiment) these pigs were slaughtered. Blood samples were taken monthly or bimonthly for total plasma cholesterol and triglycerides. At slaughter, the aorta was opened, stained with Sudan IV, and the stained area traced and measured planimetrically. Only a moderate rise occurred in plasma cholesterol and triglycerides of pigs fed high fat-high cholesterol diets. Genetically obese pigs were no more susceptible to diet-induced hypercholesterolemia and to the percentage of the surface area of the aorta stained with Sudan IV than were lean pigs. It is concluded that obesity per se is not necessarily associated with development of atherosclerosis in pigs and that innate ability to metabolize high dietary cholesterol is of greater importance than body fatness in determining the response to diet.

Weanling Landrace X Yorkshire swine were fed a basal diet or a diet containing 3% clinoptilolite (a natural zeolite) with or without 150 ppm CdCl2 or 3% zeolite NaA (a synthetic zeolite) with or without 150 ppm CdCl2 for 31 days. Hematocrit and hemoglobin were depressed significantly in animals fed Cd in the absence of zeolites, but not in their presence. Liver Cd concentration was increased dramatically by added dietary Cd but was significantly lower in animals fed clinoptilolite with Cd than in those fed Cd alone (11.4 vs 16.5 ppm). Liver Fe and Zn were decreased by dietary Cd; liver Fe was not affected significantly by clinoptilolite or zeolite NaA, but liver Zn was increased by zeolite NaA. Kidney dry matter, Zn, and Cd concentrations were increased by dietary Cd; neither clinoptilolite nor zeolite NaA affected kidney Cd concentration. Zeolite NaA increased kidney dry matter both in the presence and in the absence of dietary Cd. Plasma urea-N, K, Na, and Mg were unaffected by Cd or by either zeolite. The data illustrate the different effects of dietary clinoptilolite compared with zeolite NaA on blood plasma, liver, and kidney concentrations of minerals and provide evidence that both zeolites offer some protection against Cd-induced Fe-deficiency anemia; the magnitude of this protection and the effects of each zeolite on tissue concentrations of Cd and other materials need further quantification.

Thirty-two genetically lean and 32 genetically obese weanling (4 to 5 wk old) pigs from inter se matings of crossbreds produced by within-line matings of Duroc and Yorkshire breeds, selected for low or high backfat, were fed the following four diets for 8 wk (eight lean and eight obese pigs/diet): 10% protein -- 100 ppm Zn, 10% protein -- 200 ppm Zn, 18% protein -- 100 ppm Zn, 18% protein -- 200 ppm Zn. After 8 wk, all pigs were fed a standard 16% protein corn-soybean meal-type growing diet to a slaughter weight of about 87 kg. Lean pigs were more severely affected than obese pigs by low protein diets as measured by weight gain, plasma total protein and plasma albumin. Plasma Zn concentration was reduced in lean and obese pigs fed low protein diets. Supplemental Zn failed to increase plasma Zn in protein-deficient pigs. During repletion, weight gain of lean and obese pigs previously fed the 10% protein -- 100 ppm Zn diet was less than that of pigs previously fed other diets. The lower level (100 ppm) of Zn fed during protein depletion appeared to be associated with a negative effect on repletion weight gain of lean and obese pigs. Lean and obese pigs responded similarly during the repletion phase to earlier protein restriction. We conclude that supplementary dietary Zn does not maintain plasma Zn concentration in growing pigs fed protein-deficient diets and that repletion from dietary protein restriction is not associated with compensatory growth in genetically lean pigs.

A method was developed to measure simultaneously the 0, consumption (VO) by the whole animal and by the hepatic portal vein-drained organs (PVDO), including the gastrointestinal tract, spleen, and pancreas in conscious 3.5- to 4-month-old swine. The method was used to determine (i) the effect of feeding on hepatic portal vein blood flow rate (Qpv) and VO by PVDO and by the whole animal, and (ii) the significance of PVDO on the oxidative demand in the pig. Chronic cannulas were placed in the hepatic portal vein, carotid artery, and ileal vein. The Qpv was determined by an indicator dilution technique employing continuous constant infusion of 1% p-aminohippuric acid into the ileal vein. The VO, by PVDO was estimated by multiplying Qpv by arterial-portal vein 0, difference measured with an arterial-venous 0, difference analyzer connected to the carotid artery and portal vein cannulas. Whole animal VO, was measured with an open circuit indirect calorimeter. In seven pigs (3.5- to 4-month-old, 37.4 f 0.8 kg) trained to be fed once daily, feeding (1.2 kg of feed mixed with 1.2 liter of H,O) caused postprandial (6 hr) Qpv to increase more than 34 f 15% above the preprandial value of 34.5 f 4.2 ml. min-' . kg-' body wt. The postprandial VO, by PVDO was elevated more than 46 f 12% above the value of 1.52 f 0.20 ml.min-'.kg-' body wt observed during the preprandial period. Whole animal VO, increased 45 f 9 and 33 f 7% above the preprandial value of 6.23 f 0.57 ml. min-'. kg-' body wt for the first 6 hr and the 7 to 12 hr after feeding, respectively. Although PVDO represent only 5% of body weight, they used 25% of whole body VO,. The study clearly illustrates the significance of PVDO on the whole animal oxidative demand in conscious growing swine. (P.S.E.B.M. 1989, Vol 1901

Genetically obese and lean pigs were fed isonitrogenous-isoenergetic (digestible energy) amounts of a high or low fat diet from 25 kg body weight. Obese pigs gained less and required more feed per unit gain than lean pigs. Lean pigs were more muscular with less fat than obese pigs. Obese pigs utilized more dietary amino acids for energy (greater plasma urea N) than did lean pigs. Weight gain was similar at all intermediate periods in obese pigs fed the two diets. However, gain tended (P less than or equal to .10) to be greater and the ratio of dietary energy intake to gain tended (P less than or equal to .10) to be less in obese pigs fed high compared with low fat diets. Similar results were observed in lean pigs fed the two diets. The high fat diet produced more carcass adipose tissue deposition in both strains after 20 wk of feeding (detectable by ultrasound at 14, but not at 7 wk). Adipose tissue lipogenic rate (glucose incorporation) was similarly depressed by fat feeding in both obese and lean pigs. Obese and lean pigs both utilized dietary carbohydrate and fat differentially but there was no indication of genetic divergence regarding this utilization. In both strains of pigs, energy from the fat-enriched diet was preferentially partitioned into carcass adipose tissue.

Five experiments were done with 34 weanling and 24 growing crossbred gilts. Individually penned pigs were fed ad libitum (expt 1) or pair-fed (expt 2 through expt 5) for either 2 (expt 1 through expt 4) or 3 (expt 5) wk. Mean body weight gain and gain/feed values were significantly (P less than 0.05) greater in pigs fed carbadox (a synthetic antimicrobial). Fasting O2 consumption and CO2 production of pigs were measured during the 32- to 48-h (expt 1, 4 and 5) or during the 24- to 40-h (expt 2 and 3) postprandial periods with indirect open circuit calorimeters. Carbadox reduced O2 consumption significantly (P less than 0.05) in expt 2, but had no significant effect on CO2 production in any of the five experiments. The weight of thyroid gland and the plasma concentrations of L-3,3',5-triiodothyronine (T3) and thyroxine (T4) of pigs were not altered by carbadox. The mean weight, but not the length, of small intestine tended to be less in pigs fed carbadox. It is suggested that the growth-promoting effect of carbadox on young pigs may be associated with the weight of small intestine and its physiological processes such as metabolic rate. However, no definite effects of carbadox on whole-animal fasting metabolic rate and thyroid function could be demonstrated by the methods used in the present study.

Crossbred (Chester White x Landrace x Large White x Yorkshire) primiparous gilts were fed daily a corn-soybean meal-based gestation diet at 1.8 kg (C) or 0.6 kg (R) (6000 or 2000 kcal calculated digestible energy, DE) or a high-protein diet (RCal) at 0.6 kg (2000 kcal calculated DE) from day of mating to slaughter at 100 to 106 days of gestation. The RCal diet contained three times the concentrations of protein and of mineral and vitamin supplement present in the C diet. Body weight and ultrasonically estimated backfat depth were recorded at 0, 4, 8, and 12 weeks postcoitum. The results showed differential effects of form of diet restriction (R vs RCal) on body weight, backfat depth, relative and absolute uterine weight, and on relative kidney, stomach, and trimmed wholesale cut weights of the dam. Maternal and fetal plasma glucose and urea-N concentrations were higher in RCal than in R groups. Total uterus plus gastrointestinal tract relative weight, with or without fetuses, was lower in RCal than in R and C gilts. The ratio of uterus (with or without fetuses) weight to gastrointestinal tract weight was greater in R than in C or RCal gilts. The data are interpreted to indicate that restriction of carbohydrate-fat calories only compared with restriction of a standard diet throughout gestation in swine had a negative effect on uterine growth associated with repartitioning of nutrients to visceral organ and lean tissue growth at the expense of maternal uterine tissue and body fat conservation.

Three-week-old pigs were subjected to dietary energy or protein restriction so as to prevent weight gain over a period of 8 weeks. During the last week of restriction their responses to a novel object introduced into an exploratory test situation were measured. The malnourished pigs exhibited indifference to the object, taking longer to make contact with it, spending less time playing with it, but not showing evidence of fear or avoidance of the object or the area in which it was located. Following 6 weeks of nutritional rehabilitation, the previously malnourished pigs again displayed less approach behavior to the novel object than controls, but the effect was substantially reduced. These observations are interpreted to support our hypothesis that a major mechanism through which early malnutrition produces long-term effects on behavior is by disturbing those behaviors required for gathering information from the environment.

The nutrient compositions of various fermented manures were compared. Large differences in the mineral concentration were observed. There were no important differences among the amino acid composition of S. spirulina grown on the different nutrient media. All were low in methionine, but were rich in glutamic acid, aspartic acid, arginine, and leucine. The crude protein content was 71.8-60.1%. Considerable contamination of the waste-grown algae with yeast, fungi, and sporogenous bacteria was experienced.

Developmental changes in growth hormone levels during protein or energy malnutrition was studied in weaned pigs. Three or 4 week old pigs from control dams were fed a control diet (18% protein), an energy-restricted diet (18% protein) or a low protein diet (6% protein) for 8 weeks. Energy restriction was achieved by feeding the control diet in amounts that allowed very little growth. After the restriction period, all pigs were fed the control diet ad libitum for another 8 weeks. Blood samples were collected at intervals throughout the experiment and the plasma was analyzed for growth hormone by radioimmunoassay. Post weaning protein deprivation resulted in higher growth hormone levels during the restriction period as compared to control pigs or pigs with a restricted energy intake. J. Nutr. 106: 947-951,1976.

The effects of restricting protein intake on plasma insulin were studied in pregnant pigs, fetuses and the developing offspring. Pregnant pigs were fed diets containing 18%, 3% or 0.5% protein throughout the gestation period. At 10, 13 and 15 weeks of gestation, fetuses were removed from the uterus after bleeding the dam. Plasma samples were used for insulin determination by a radioimmunoassay procedure. At week 15 of gestation, plasma insulin levels were significantly higher in pregnant pigs fed 18% protein and also in their fetuses than in the other two groups. There was a high correlation between fetal insulin level and fetal growth rate (r = 0.84). Two-day-pld pigs from another set of pregnant pigs fed the diet containing 18%, 3%, or 0.5% protein during gestation were cross-fostered to control nursing dams and weaned at 4 weeks of age to a standard diet. Plasma smaples obtained at regular intervals were used for insulin determination. Offspring of pigs fed 0.5% protein during gestation had consistently low insulin levels in postnatal life in spite of cross-fostering and standard feeding after weaning. It appears that one of the stimuli which control maternal insulin secretion and placenta transfer is the maternal protein intake while severe maternal protein restriction might contribute to the low levels of insulin in the progeny during postnatal life.

A 2 X 3 factorial arrangement was used in each of two trials with two levels of floor space allowance (.25, .13 m2/pig) and three dietary treatments (basal, basal + 660 ppm vitamin C, basal + 55 ppm carbadox). The reduction in floor space allowance was achieved in trial 1 by doubling the number of pigs/pen from eight to 16 and in trial 2 by reducing the size of pens by half. An 18% protein starter diet was used as the basal diet. Total numbers of pigs used were 216 in trial 1 and 144 in trial 2. Pigs were weaned between 4 and 5 wk of age (7.5 kg average wt) and fed ad libitum for 28 d. Reducing floor space allowance caused a (P less than .05) reduction in weight gain of weanling pigs in both trials. When the reduction of floor space allowance was done by increasing number of pigs/pen (trial 1), pigs responded with a significantly reduced feed intake with no change in efficiency of feed utilization. However, when floor space allowance was reduced by changing the size of the pen (trial 2), feed intake of pigs was not affected but efficiency of feed utilization was reduced significantly. Neither form of crowding affected vitamin C concentration in adrenal glands and weights of adrenal glands, spleen and thymus. Dietary supplementation of carbadox, but not vitamin C, produced significantly greater weight gain, feed efficiency, and spleen weight of pigs in both trials. Although there was no interaction between crowding and dietary treatment in affecting the performance of pigs, supplemental carbadox improved the performance of crowding-stressed pigs by maintaining an adequate level of feed intake and improving feed efficiency, whether crowding was caused by increased pig density or by reduced pen size. No significant differences in phytohemagglutinin (PHA) skin test response or in the neutrophil-to-lymphocyte ratio (N/L) were observed among treatments in trial 1, while a significantly reduced response to PHA and a higher N/L were detected in crowding-stressed pigs in trial 2.

Fifty-six castrated male progeny of crossbred (Chester White x Landrace x Large White x Yorkshire) dams fed an adequate diet (control, C), a control diet fed at one-third of C (restricted, R), or diets severely deficient in protein (PF) or restricted in nonprotein calories (RCal) were killed at age 25 weeks. Dams were fed their respective diets in the following regimens: C, 1.8 kg (6000 kcal daily) throughout pregnancy; R, 0.6 kg of C diet daily for 70 days, then 1.8 kg of C daily to parturition at about 114 days; PF, 1.8 kg of a "protein-free" diet (less than 0.2% protein) throughout pregnancy; RCal, 0.6 kg daily (2000 kcal) of a diet containing three times the concentration of protein, minerals, and vitamins provided by the C diet for 70 days, then 1.8 kg of C daily to parturition. All dams were fed an adequate diet ad libitum through a 28-day lactation. Castrated male progeny were assigned to one of two replicates based on birth date and fed a corn-soybean meal diet ad libitum from weaning to age 25 weeks, supplemented from age 10 to 12 weeks with 0, 110, or 220 mg/kg of thyroprotein (iodinated casein). Cerebrum weight was unaffected by maternal diet, despite a significant (P less than 0.001) reduction in body weight of progeny of PF dams compared with other groups, resulting in a higher relative cerebrum weight in progeny of PF dams than in progeny of C, R, and RCal dams. Absolute and relative weights of RNA, DNA, and total protein in cerebrum were unaffected by maternal diet. Thyroprotein supplementation to the diet of the progeny had no effect on cerebrum weight or its protein or nucleic acid content. It is concluded that maternal protein deprivation but not restriction of feed or nonprotein calorie intake to one-third of recommended allowance during gestation results in stunting of body weight in young adult progeny but does not affect cerebrum weight, cerebrum cell number (DNA), or protein synthetic activity (RNA), or RNA-to-protein ratio.

Pigs (Yorkshire) were subjected to protein-energy mal nutrition in the following manner: 3- or 4-week-old pigs from control dams were fed a control diet (18% protein), an energy-restricted diet (18% protein), or a low protein diet (6% and 3% protein) for 8 weeks. Energy restriction was achieved by feeding the control diet in amounts that al lowed some growth, but only to an extent equal to the low protein diet being matched. After the restriction period, all pigs were fed the control diet for another 8 weeks. Blood samples were collected at intervals from the superior vena cava. Plasma samples were analyzed for corticosteroids in all groups and for free cortisol in the controls and 3% protein groups. No sig nificant differences were found for total plasma corticosteroids among all groups. Free cortisol was found significantly higher in the 3% group com pared to the controls. An ACTH test was performed with depleted and recovered pigs of the 3% protein group and controls. No differences were found among controls, depleted and recovered pigs. J. Nutr. 106: 952-957,1976.

The effects of low protein diets on plasma growth hormone were studied in pregnant pigs, fetuses and the developing progeny. Preg nant pigs were fed 18%, 3% or 0.5% protein diet throughout the gestation period. At 10, 13 and 15 week of gestation, fetuses were removed from the uterus after the dam had been bled to death. Plasma samples were used for growth hormone determinations. In a second experiment, 2-day old pigs from another set of pregnant pigs fed the diet containing 18%, 3% or 0.5% protein during gestation were cross-fostered to control nursing dams and weaned at 4 weeks of age to a standard diet. Plasma obtained at regular intervals was used for growth hormone determination. Plasma growth hormone was significantly higher in dams fed 0.5% protein after week 13 of gestation. High growth hormone (ten times the dam GH level) was ob served in all fetuses irrespective of maternal dietary manipulation. Offspring of severely protein deprived pigs (0.5% protein) had significantly elevated growth hormone levels up to 12 weeks of age in spite of cross fostering to a control dam after birth. The data suggest that there is little or no effect of maternal protein restriction on fetal growth hormone levels but the per sistent high growth hormone levels in the progeny of severely malnourished pigs indicate a possible impairment of the production, release or catabolism of growth hormone and/or its releasing factor. J. Nutr. 106: 940-946, 1976.

SummaryThe distribution of injected 32P was studied in the mildly hyperammonemic chick and rat. Ammonia toxicity in the chick resulted in decreased accumulation of 32P in the tibia (p

SummaryDietary magnesium, potassium and protein interactions were studied in weanling rats. Growth rate, efficiency of feed utilization, and blood serum magnesium and calcium levels were significantly lower in rats fed a magnesium-deficient diet than in those fed a similar magnesium-adequate diet. A diet containing 4 times as much potassium (8132 mg/kg) increased the serum magnesium level 60% after 28 days (1.0 vs. 1.6 mg%) and 90% after 56 days (0.9 vs 1.7 mg%) indicating an inhibition by potassium of the reduction in serum magnesium associated with consumption of magnesium-deficient diet. Typical gross magnesium deficiency symptoms, including reddened ears and paws and convulsions lasting 1–5 minutes were observed, however, in all groups fed low magnesium diets regardless of potassium level. Diets containing 20% protein produced significantly greater growth rate than those containing 10% in the presence of adequate magnesium but not during magnesium deficiency. No histological lesions associated with tr...

Seventy-six young adult nongravid female rats of the Carworth strain were used in two experiments to study the effect of dietary protein deprivation on body weight, feed consumption, body composition and serum protein concentration. Semi- purified diets containing glucose, corn oil, vitamins and minerals with or without casein (protein-free = PF, 14% casein = C) were fed ad libitum in both experiments to rats caged in individual wire-bottom cages. Feeding the PF diet for up to 26 days resulted in a continuous weight loss over the entire period. The average loss in body weight as a percentage of initial weight of PF rats in experiments 1 and 2 was 32.9 and 25.7, respectively. Weight loss during 9 days in rats fed the PF diet was restored within 8 days following transfer to the C diet. Feed consumption was reduced only moderately by the PF diet, suggesting a large loss of ingested calories by excretion or metabolism to carbon dioxide and water. Body composition data supported this and indicated a greater relative loss of body energy than of body protein in PF rats. Blood serum protein concentration was reduced moderately (P < 0.05) in rats fed the PF diet. The absolute loss of serum protein may have been greater than suggested by the concentration if it is assumed that there was a reduction in blood volume associated with the observed weight loss. Blood serum protein concentration therefore does not appear to be as sensitive an index of protein nutrition in the adult as in the young animal. Final body energy, protein and water content were less in PF rats than in C rats in experiment 2 by an average of 176.5kcal (36%), 10.9 g (23%) and 41.7 g (28% ), respectively. Energy concentration (kilocalories per gram dry weight) was 11% greater in C than in PF rats (5.8 versus 5.2 kcal/g). These data indicate that the adult female nongravid rat can survive a loss of at least one-third of body energy and one-fourth of body protein induced by protein deprivation without developing severe hypoproteinemia, emaciation and edema. The effect of dietary protein depriva- gravid animals. The experiments reported tion on reproductive performance has been here describe the effects of protein depri- studied extensively in the rat (1-3) but vation on body weight, voluntary feed con- only limited data are available on its effects sumption, serum protein level and body on the nongravid female rat. Protein dep- composition of adult nongravid female rats, rivation reduces the incorporation of amino EXPERIMENTAL PROCEDURE acids into protein in muscle and increases incorporation in liver (4). It results in a General. Female rats of the Carworth three- to fourfold increase in liveramino strain were used in two experiments. Rats acid-activating enzymes (5). The nitro- were assigned randomly to dietary treat- gen concentration of liver from protein- ment at 12 to 14 weeks of age, at body deprived rats is reduced and body weight weights averaging approximately 225 and loss is greater than in rats fed an equal 215 g, in experiments 1 and 2, respectively, intake of an adequate diet (6). Informa- Jn each experiment rats were kept in in- tion on changes in body weight and com- dividual wire-bottom cages and offered position of adult animals deprived of pro- water ad libitum from glass water bottles tein is of importance in predicting the attached to the cage, and feed ad libitum effects of such dietary restriction in other from porcelain feed dishes designed for species, including man, and in providing minimum feed wastage. Feed consumption a basis for comparison of the effects of and body weight were recorded every sec- protein deprivation in gravid versus non- Receivedfor publicationJuly 17, 1968.

SummaryThe chronological events occurring in blood after intoxicating doses of ammonium carbonate were studied using the suckling pig. Physical manifestations included vomiting, hyperventilation, hypersensitivity to sound, convulsions, and tetany followed by death in some cases. Blood glucose, dihydroxyacetone-P, pyruvate and lactate were raised indicating failure to decarboxylate pyruvate. Elevated blood ketone bodies indicated increased fat catabolism as a result. Consistent rise in blood pentose may either be due to an inhibition of the pentose phosphate pathway or an increased metabolism of glucose via this pathway to make up for reducing power lost through impairment of the TCA cycle.

The intent of this study was to determine if release of ammonia in the intestines with the subsequent complex formation with magnesium and phosphorus could interfere with the absorption of substances transported into the body by energy-requiring processes. The absorption of glucose, 45Ca2+and 32PO43~ from the ligated duodenal loop of the chick was significantly lower in the presence of NH4C1than for animals not given the NH4C1in the test dose. The accumulation of "Ca and 32Pin the tibia was also significantly lower as the result of NH4C1administration. Urea, equimolar to the NH4C1,showed no effect on intestinal absorption or bone accumulation, indicating little or no hydrolysis of urea in the chick duodenum in the 20-minute test period. Glycine increased glucose absorption, while lysine decreased 32P absorption without affecting the 32Puptake by the tibia. It was postulated that ammonia immobilized inorganic phosphate through complex formation and thus reduced 32P absorption. The depletion of the inorganic phosphorus could lead to insufficient available high energy phosphate for energy-requiring transport processes for glucose and cal cium. J. Nutr. 102: 1513-1518, 1972.