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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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

This study was conducted to test the hypothesis that maternal dietary protein deficiency decreases amino acid availability to the fetus, thereby contributing to retarded fetal growth. 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 maternal and fetal blood samples as well as amniotic and allantoic fluids were obtained for analyses of amino acids, ammonia and urea. Dietary protein restriction decreased (P < 0.05) the following: 1) maternal plasma concentrations of urea at d 40 and 60 of gestation; 2) fetal plasma concentrations of alanine, arginine, branched-chain amino acids (BCAA), glutamine, glycine, lysine, ornithine, proline, taurine, threonine and urea at d 60 of gestation; 3) amniotic and allantoic fluid concentrations of urea at d 40 and 60 of gestation; and 4) allantoic fluid concentrations of alanine, arginine, BCAA, citrulline, cystine, glycine, histidine, methionine, proline, serine, taurine, threonine and tyrosine at d 40 of gestation, in gilts of both genetic lines. At d 60 of gestation, protein deficiency decreased (P < 0.05) allantoic fluid concentrations of arginine, cystine, glycine, taurine and tyrosine in low line gilts and of cystine, glutamine, ornithine, serine, taurine and tyrosine in high line gilts. Low line and high line gilts also differed remarkably in allantoic fluid concentrations of arginine, glutamine, ornithine and ammonia at d 40 and 60 of gestation. Our results suggest the following: 1) protein-deficient gilts maintain maternal plasma concentrations of amino acids by mobilizing maternal protein stores and decreasing oxidation of amino acids during the first half of gestation; 2) protein deficiency may impair placental transport of amino acids from the maternal to the fetal blood; and 3) low line and high line gilts differ in fetal amino acid metabolism. Decreases in concentrations of the essential and nonessential amino acids in the fetus may be a mechanism whereby maternal dietary protein restriction results in fetal growth retardation. [ABSTRACT FROM AUTHOR]

To determine the effect of severe chronic protein deficiency on protein synthesis in different tissues and total protein in plasma, and on plasma biochemical constituents involved in amino acid metabolism, we fed diets containing either 20 or 3% protein to two groups of four age-matched piglets. After consuming the diets for 8 wk, the pigs received a primed-constant infusion of 2 H3-leucine for 8 h to measure the fractional synthesis rates (FSR) of tissue protein and total protein in plasma. Plasma urea and amino acid concentrations, particularly indispensable amino acids, were significantly lower in protein-deficient pigs. Fractional protein synthesis rates were lower in skin by 66% (P < 0.01), in jejunal mucosa by 50% (P < 0.05), in masseter muscle by 40% (P < 0.05), and in liver by 25% (P < 0.02); the fractional synthesis rate of the longissimus muscle was not different than controls. Although plasma protein concentration was significantly (P < 0.01) lower in protein-deficient pigs, the fractional synthesis rate of the total intravascular plasma protein pool was not different. We conclude that adaptation to a low protein diet involves a reduction in the rate of protein synthesis in most body tissues, with the most marked changes occurring in skin and intestine, two tissues which frequently exhibit severe functional impairment in protein malnutrition.

Dietary cholesterol in infancy may alter cholesterol metabolism and the propensity to develop atherosclerosis. This study examined the effects of a 1% cholesterol diet (HC) vs. a no-cholesterol diet (NC) during the first 2 mo of life on pigs selectively bred for leanness or obesity. Three lean and three obese pigs received the no-cholesterol diet, and four lean and four obese pigs received the 1% cholesterol diet from d 1. Lean and obese pigs fed the no-cholesterol diet showed no increase in serum lipid concentrations, nor did they develop atherosclerosis. Obese pigs fed the 1% cholesterol diet developed significantly higher serum total cholesterol (TC) and high density lipoprotein cholesterol (HDL-C) at 35 d than lean pigs fed the 1% cholesterol diet. By d 55, only HDL-C remained significantly higher in the obese pigs, resulting in a higher (P < 0.1) TC/HDL-C ratio in the lean pigs. Atherosclerotic plaque formation in the aorta was more extensive in the lean pigs. Cholesterol synthesis measured in vivo and at termination was equally suppressed in lean and obese pigs fed the 1% cholesterol compared with pigs fed the no-cholesterol diet. We conclude that genetic differences in the response of these lean and obese pigs to a high cholesterol diet render obese pigs less susceptible to atherosclerosis despite higher serum TC concentrations. The persistent elevation of HDL-C in obese pigs is the most likely mechanism of protection.

Three-wk-old genetically lean or obese pigs were used in two experiments to determine the changes in body composition, visceral organs and brain in response to severe protein deficiency. In Experiment 1, 16 obese pigs were fed an adequate (A, 21% protein, 3% fat) or a protein-deficient (D, 5% protein, 23% fat) diet for 7 wk. One-half of each group was killed at 7 wk, and the remainder of each group was fed the A diet for an additional 8 wk. At 7 wk, pigs fed D contained a higher percentage of fat than those fed A (P < 0.01); after 8-wk of repletion, body composition of the two groups was similar. Duodenum, jejunum, and ileum of the protein-deficient pigs had severely atrophic villi, submucosal edema, and atrophic muscle layers; after 8 wk of repletion, however, microscopic architecture of the gastrointestinal tract was restored to normal. Absolute cerebrum weight at 7 wk, but not after 8 wk repletion, in the pigs fed D were significantly less than in pigs fed A, indicating reduced brain cellularity after 7 wk of protein restriction, but not after 8 wk repletion. In Experiment 2, genetically obese (O, n = 8) and lean (L, n = 8) pigs consumed the A or D diet ad libitum for 10 wk. L and O pigs responded similarly to protein deficiency; D pigs were fatter than A pigs and plasma constituents, bone mineral content, bone mineral density and most organ weights revealed no interactions between diet and genotype. The pig model system used in these experiments enabled the isolation of protein deficiency from infectious disease, parasites and social environmental stimulation that may confound interpretation of human infant malnutrition experiments. The data suggest that genetically controlled body fatness is not a major determinant in the response of the infant pig to severe protein deficiency.

We studied the effect of dietary cholesterol on tissue cholesterol synthesis in 10 genetically lean pigs using the 2H2O incorporation method. Five pigs were fed a diet containing 0% cholesterol (controls) and five were fed a diet containing 0.5% cholesterol (cholesterol-fed) from d 1 to d 54 of age. From d 30 to d 54, they received 2H2O and cholesterol synthesis was determined by measuring deuterium enrichment in erythrocyte cholesterol. All pigs were killed on d 54 and liver, ileum, jejunum, kidney, adipose tissue, muscle, and cerebrum were collected for measurement of free and esterified cholesterol and of the deuterium content of tissue free cholesterol. In vivo cholesterol synthesis was inhibited by dietary cholesterol as reflected by a decrease in fractional synthesis rate from 16.8 +/- 1.7%/d in controls to 2.3 +/- 1.1%/d in cholesterol-fed pigs. Cholesterol feeding raised cholesterol ester concentration in plasma, liver, and other tissues. Deuterium enrichment of free cholesterol in tissues, such as liver, was reduced from 11.98 +/- 2.82 milli atom percent excess in controls to 1.83 +/- 1.14 in cholesterol-fed pigs. Greater cholesterol intake did not inhibit cholesterol synthesis in the cerebrum. Deuterium enrichment levels of cholesterol in plasma and liver were similar to those in other tissues except for brain, suggesting an equilibration of cholesterol between the liver and most extrahepatic tissues. The control of cholesterol synthesis in brain appears to be independent of that in liver and other tissues of the body.

We hypothesized that, in pigs selected for low (L) or high (H) serum cholesterol for four generations, neonatal endogenous cholesterol synthesis would be sufficient to meet requirements for brain and body growth. In Experiment 1, eight 16-wk-old L pigs received a diet with or without 200 mg cholesterol/100 g diet for 35 d. Supplemented pigs grew approximately 25% faster and had a significantly greater concentration of free cholesterol in the cerebrum. In Experiment 2, 16 H and 16 L newborn pigs were fed a milk replacer with or without 200 mg cholesterol/100 g diet for 28 d. Pigs fed cholesterol had greater average daily gain (P < or = 0.09), significantly reduced liver 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity, and significantly increased cerebral cholesterol content than pigs not fed cholesterol. One of three indices of exploratory behavior was significantly greater in the L pigs that received cholesterol compared with L pigs that did not receive cholesterol. These data suggest that these neonatal pigs are unable to produce sufficient cholesterol to meet requirements for normal growth and brain development and are dependent on dietary cholesterol in milk.

Protein deficiency during pregnancy affects fetal development. The critical period, when the fetus is most susceptible to maternal protein deficiency and its effect on neonatal growth, is unknown. Therefore, we studied the effect of a protein-restricted diet during early and late pregnancy and throughout pregnancy on growth of pigs from birth to market weight. Sows were fed a control (13% protein) or protein-restricted (0.5% protein) diet throughout pregnancy or protein-restricted diet from d 1 to 44, then control diet to term or control diet from d 1 to 81, then the protein-restricted diet to term. In Experiment 1, birth weights were measured, and 12 pigs/diet group were weaned at 4 wk and raised to market weight. Feeding the protein-restricted diet throughout pregnancy reduced birth and slaughter weights, whereas the control followed by protein-restricted and protein-restricted followed by control diets reduced only birth weight relative to controls. Indices of carcass lean were reduced in the protein-restricted piglets, with carcass fat not affected. In Experiment 2, control and control-protein-restricted litters were reduced to six piglets and 3/litter cross-fostered to a sow of the other treatment group. After weaning at 4 wk, 4 piglets/group were individually fed to 8 wk. The control and control followed by protein-restricted diet fed piglets had similar weights at birth, but piglets raised by a control-protein-restricted sow tended to weight less at weaning than their littermates raised by a control sow. After weaning, these piglets had greater feed intakes relative to other groups and there were no weight differences by 8 wk.(ABSTRACT TRUNCATED AT 250 WORDS)

The impact of cholesterol exposure in early life on later cholesterol metabolism is not clearly understood. Sixteen newborn genetically lean and obese pigs were fed 0 or 5.0 g cholesterol/kg diet (0 or 0.5%) (liquid diets for 12 d, dry diets thereafter) for 33 d, after which they were all fed 10.0 g cholesterol/kg diet (1.0%) for 23 d. All animals were killed on d 56 and whole-body protein, fat and water were determined on the ground carcass. Dietary cholesterol had no consistent effect on growth rates or body composition. Mean fat content of lean pigs was 15.1% compared with 22.7% for obese pigs; corresponding values were 14.8 and 14.4% for protein and 65.5 and 58.3% for water. Concentrations of plasma total cholesterol, HDL cholesterol and apolipoproteins B and A-1 were increased by 0.5% dietary cholesterol in obese but not in lean piglets, although dietary cholesterol caused HDL and LDL size distribution profiles to shift toward larger-sized components in both strains. Plasma total cholesterol and apolipoprotein B concentrations rose two- to eightfold in all groups after the 1% cholesterol diet was consumed; these changes were accompanied by shifts in LDL and HDL size distribution profiles towards larger-sized components. With 1.0% cholesterol in the diet of all groups, HDL cholesterol concentration increased by approximately 50% in both groups of lean pigs and in obese pigs previously fed cholesterol, but did not increase further in obese pigs previously fed 0.5% cholesterol. The magnitude of the hypercholesterolemic response in lean pigs was blunted by previous exposure to 0.5% dietary cholesterol, but the response was accentuated in obese animals that had been previously exposed to 0.5% dietary cholesterol. These data provide evidence that genetic differences between obese and lean pigs affect their serum lipoprotein responses to high cholesterol intake.

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.

The effects of low protein diets on plasma growth hormone were studied in pregnant pigs, fetuses and the developing progeny. Pregnant 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 observed in all fetuses irrespective of maternal dietary manipulation. Offspring of severely protein deprived pits (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 persistent 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.

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.

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.

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)

Rats and swine were restricted in feed during pregnancy to determine the effect on postnatal growth and development of the progeny. Restriction of rats to 50% of preconception feed intake during the first 2 wk of gestation was associated with higher body weight of the progeny at 21 wk postpartum than was ad libitum feeding throughout gestation. However, maternal intake during gestation had no effect on perirenal and gonadal fat weight or adipocyte size in male and female offspring at 160 d of age. Restriction of swine to one-third of recommended feed intake during the first 10 wk of pregnancy was associated in the progeny with less perirenal and subcutaneous backfat and smaller adipocytes in depot fat compared with progeny of adequately fed swine. It is concluded that feed restriction of pregnant rats to one-half of preconception intake for the first two-thirds of pregnancy results in increased weight gain in the resulting progeny while restriction of swine to one-third of the recommended feed allowance during the first two-thirds of pregnancy results in reduced postweaning weight gain and decreased fat accretion during young adulthood.

Finishing barrows (average initial weight 55.5 +/- 2.4 kg) were used to determine the effects of high dietary fiber or protein on performance, visceral organ weights and large intestine microbial populations and to monitor the duration of regression of swine visceral organ mass and microbial populations to control values following transfer from the high fiber or high protein diet to the control diet. Four pigs from each diet were killed on d 17, 34, 48 and 66. From d 34 until slaughter 14 and 32 d later, all remaining pigs were fed the control diet ad libitum. High fiber resulted in significantly higher relative weight of the total gastrointestinal tract after 34 d and higher relative stomach weight up to d 48. Compared with the control diet, the high protein diet resulted in increased relative liver and kidney weights up to d 48. The number of proteolytic and cellulolytic bacteria increased in the colon contents of pigs fed a high protein or high fiber diet, respectively, but declined to below control values within 14 d of transferring pigs from the high protein or high fiber diet to the control diet. The results indicate that diet composition plays a more specific role in visceral organ hypertrophy than can be explained by the normal relative changes in organ size as body weight increases. Thus, high dietary fiber and protein may indirectly increase the animal's maintenance requirement by causing a repartitioning of nutrients from the edible carcass to the visceral organs.

Sixty-one primiparous Sprague-Dawley female rats were fed an adequate diet containing 5% protein (experiment 1) or 8% protein (experiment 2) throughout gestation. Low dietary protein reduced individual pup birth weight in both experiments (P less than .01 in experiment 1 and P less than .10 in experiment 2) and drastically decreased early postnatal survival in experiment 1. Weaning weight of survivors was reduced by gestation protein deprivation in experiment 1 but no in experiment 2. Male and female progeny surviving to weaning in experiment 1 and randomly selected progeny from each maternal treatment in experiment 2 were caged individually and fed ad libitum and nutritionally adequate corn-soybean meal-type diet throughout the entire life span. Body weight were recorded monthly beginning in young adulthood and continuing until death. Life span (in days) was recorded for each rat. Mature body weight of male and female progeny of dams fed restricted protein during gestation was less in both experiments than that of offspring from dams fed an adequate diet (P less than .01). There was no effect of prenatal nutrition on life span in either experiment, but females lived significantly longer than males in both experiments (p less than .05). It is concluded that maternal protein restriction during gestation of a magnitude large enough to reduce pup birth weight causes a significant reduction in mature body size of the progeny without affecting longevity in the rat.

Interactions of a high fat-high cholesterol diet with low and high dietary protein levels were tested in genetically obese and lean growing pigs. Sixty-four growing swine (32 obese and 32 lean) were utilized in a 9-wk experiment in which four diets were fed in a 2 X 2 factorial arrangement with two levels of plant protein (8 and 16%) and two levels of fat and cholesterol (0 added or 11% beef tallow-3% dried egg yolk added). Daily gain and gain-to-feed ratio were significantly reduced by low protein (P less than 0.01) and increased by high fat-high cholesterol. Obese pigs gained weight faster than lean pigs but were less efficient in feed utilization (P less than 0.02) except when consuming low protein diets (P less than 0.001). Plasma cholesterol was increased by low protein (P less than 0.01) and by high fat-high cholesterol (P less than 0.02); highest values were in pigs fed low protein-high fat-high cholesterol. Lean pigs showed a greater rise than obese pigs in plasma cholesterol when fed low protein diets, reflecting a higher dietary protein requirement for lean pigs as indicated by plasma total protein, albumin and urea nitrogen (urea-N) responses to diet. Percentage of aortic surface area stained by Sudan IV tended to be higher in lean than in obese pigs but the difference was not statistically significant (P less than 0.25). The data show the hypercholesterolemic effect of dietary protein restriction in growing swine and establish that genetic differences related to body composition and quantitative protein requirement affect the response.

Two experiments were conducted with pigs to investigate changes in plasma insulin levels during protein-energy malnutrition. Three or four week old pigs were fed a control diet (18% protein), an energy-restricted diet (19% protein) or a low protein diet (6% protein) for 8 weeks. Energy restriction was achieved by feeding the control diet in amounts that allowed some growth, but only to an extent equal to the low protein diet. At the end of the restriction period, all pigs were fed the control diet for another 8 weeks. Blood samples from the superior vena cava were collected at intervals throughout the experimental period. Plasma samples were analyzed for insulin by radioimmunoassay. Protein restriction after weaning resulted in persistently low insulin levels during depletion and rehabilitation periods, while high levels of plasma insulin were observed in energy-restricted pigs only during the depletion period compared to pigs fed the control diet.

Genetically obese (O), and lean (L) and contemporary (C) primiparous swine were assigned from day 30 to 40 of pregnancy to parturition to one of two dietary treatments: 1) 1.8 kg daily (6000 kcal DE) digestible energy, and 2) 0.6 kg daily (2000 kcal DE) of a standard corn-soybean meal-based diet. O gilts weighed less and were fatter at week 16 than L or C gilts. L and C gilts fed the low diet intake maintained constant body weight throughout pregnancy while O gilts gained approximately 10 kg. All gilts fed adequate energy gained weight. Plasma free fatty acids were higher and triglycerides were lower in pregnant gilts fed restricted energy. Plasma cholesterol and blood glucose appeared to be unaffected by genetic background, suggesting that genetic propensity to obesity is not necessarily associated with hypercholesterolemia or hyperglycemia. Pig birth weight was reduced by maternal feed restriction only in O and C pigs; survival was higher in progeny of O dams than in those of L and C dams. Maternal energy restriction had no effect on survival in L, C, or O pigs. Preweaning growth of C but not of L or O progeny was adversely affected by maternal feed restriction. The data illustrate the significance of genetic X gestation energy interactions in dam and progeny traits and suggest that a consideration of genetic background is essential in evaluating response criteria related to feed restriction during pregnancy.

Pigs (Yorkshire) were subjected to protein-energy malnutrition 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 allowed 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 significant differences were found for total plasma corticosteroids among all groups. Free cortisol was found significantly higher in the 3% group compared 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.

Developmental changes in growth hormone levels during protein or energy malnutrition was studied in weaned pigs. Three or 4 weeks 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.