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Dietary betaine may reduce carcass fat in growing pigs. We explored the effects of betaine on short-term growth and in vivo and in vitro fatty acid oxidation. Pigs were housed in metabolism crates and fed diets containing either 0% (control), 0.125% or 0.5% betaine at 80% of ad libitum energy intake. Fatty acid oxidation was measured during intravenous infusions of 1-(13)C-palmitate and in hepatocytes incubated in the presence or absence of betaine and carnitine. CO2 and palmitate isotopic enrichments were determined by mass spectrometry. Pigs consuming 0.125% and 0.5% betaine for at least 9 days had growth rates that were 38% and 12% greater than controls, respectively. Feed efficiency was also improved with betaine. Fasting increased palmitate oxidation rates 7-8-fold (P < 0.01), but betaine had no effect in either the fed or fasted state (P > 0.1). For hepatocytes, carnitine but not betaine enhanced palmitate oxidation. This response suggests that previously observed reduction in adipose accretion must be via a mechanism other than oxidation. Betaine had no effect on plasma non-esterified fatty acids or urea nitrogen. Under the confinement conditions in this study, dietary betaine improved animal growth responses, but it had no apparent effect on either whole body or hepatic fatty acid oxidation.

The effect of multiple lipopolysaccharide (LPS) challenges in swine undergoing long-term treatment with porcine somatotropin (PST) was determined. Changes in aspartate serine transaminase (AST) occurred only at 24h following the first LPS challenge dose (P<0.05), while PST treatment moderated any change from occurring. Nonesterified free fatty acid (NEFA) levels were elevated in PST treated animals for the first 3 days following daily LPS treatment (P<0.05), while LPS treatment alone had no effect on plasma NEFA levels. Plasma urea nitrogen (PUN) levels were unchanged by LPS following the initial LPS challenge, but were decreased following the second challenge dose (P=0.014). These changes were long lasting, with a return to normal PUN levels not evident until Day 6. The PST treatment mitigated changes in PUN (P<0.05) when LPS was administered. Haptoglobin plasma levels, along with lipid peroxide production were not affected by LPS challenge or PST administration. LPS challenge reduced the levels of immunoreactive heat shock protein 70 (HSP70) throughout the entire challenge period (P<0.001). PST-LPS animals had normal levels of this protein. The results of the present study demonstrate that long-term PST treatment mitigates the adverse effects of subchronic LPS administration.

To differentiate the effect of somatotropin (ST) treatment on protein metabolism in the hindquarter (HQ) and portal-drained viscera (PDV), growing swine (n = 20) treated with ST (0 or 150 microg x kg(-1) x day(-1)) for 7 days were infused intravenously with NaH(13)CO(3) and [(2)H(5)]phenylalanine and enterally with [1-(13)C]phenylalanine while in the fed state. Arterial, portal venous, and vena cava whole blood samples, breath samples, and blood flow measurements were obtained for determination of tissue and whole body phenylalanine kinetics under steady-state conditions. In the fed state, ST treatment decreased whole body phenylalanine flux, oxidation, and protein degradation without altering protein synthesis, resulting in an improvement in whole body net protein balance. Blood flow to the HQ (+80%), but not to the PDV, was increased with ST treatment. In the HQ and PDV, ST increased phenylalanine uptake (+44 and +23%, respectively) and protein synthesis (+43 and +41%, respectively), with no effect on protein degradation. In ST-treated and control pigs, phenylalanine was oxidized in the PDV (34-43% of enteral and arterial sources) but not the HQ. In both treatment groups, dietary (40%) rather than arterial (10%) extraction of phenylalanine predominated in gut amino acid metabolism, whereas localized blood flow influenced HQ amino acid metabolism. The results indicate that ST increases protein anabolism in young, growing swine by increasing protein synthesis in the HQ and PDV, with no effect on protein degradation. Differing results between the whole body and the HQ and PDV suggest that the effect of ST treatment on protein metabolism is tissue specific.

The purpose of this study was to examine the effects of dietary betaine over a range of concentrations (between 0 and 0.5%) on growth and body composition in young feed-restricted pigs. Betaine is associated with decreased lipid deposition and altered protein utilization in finishing pigs, and it has been suggested that the positive effects of betaine on growth and carcass composition may be greater in energy-restricted pigs. Thirty-two barrows (36 kg, n = 8 pigs per group) were restrictively fed one of four corn-soybean meal-skim milk based diets (18.6% crude protein, 3.23 Mcal ME/kg) and supplemented with 0, 0.125, 0.25, or 0.5% betaine. Feed allotment was adjusted weekly according to BW, such that average feed intake was approximately 1.7 kg for all groups. At 64 kg, pigs were slaughtered and visceral tissue was removed and weighed. Carcasses were chilled for 24 h to obtain carcass measurements. Subsequently, one-half of each carcass and whole visceral tissue were ground for chemical analysis. Linear regression analysis indicated that, as betaine content of the diet was elevated from 0 to 0.5%, carcass fat concentration (P = 0.06), P3 fat depth (P = 0.14) and viscera weight (P = 0.129) were decreased, whereas total carcass protein (P = 0.124), protein deposition rate (P = 0.98), and lean gain efficiency (P = 0.115) were increased. The greatest differences over control pigs were observed in pigs consuming 0.5% betaine, where carcass fat concentration and P3 fat depth were decreased by 10 and 26%, respectively. Other fat depth measurements were not different (P > 0.15) from those of control pigs. In addition, pigs consuming the highest betaine level had a 19% increase in the carcass protein:fat ratio, 23% higher carcass protein deposition rate, and a 24% increase in lean gain efficiency compared with controls. Dietary betaine had no effects (P > 0.15) on growth performance, visceral tissue chemical composition, carcass fat deposition rate, visceral fat and protein deposition rates, or serum urea and ammonia concentrations. These data suggest that betaine alters nutrient partitioning such that carcass protein deposition is enhanced at the expense of carcass fat and in part, visceral tissue.

Fatty acid-free albumin has been the standard carrier for intravenous infusion of fatty acids to study in vivo lipid metabolism. However, subjects can have adverse reactions to infusion of albumin. We sought an alternative to albumin as a carrier for intravenous infusion of fatty acids, using the pig as a model. Cyclodextrins are naturally occurring water-soluble molecules that can serve as carriers for lipid-soluble compounds. 13C-palmitate was complexed to either 20% methyl-beta-cyclodextrin, 20% 2-hydroxypropyl-beta-cyclodextrin, or 5% porcine albumin (isotopic purity of infusates: 99.22+/-0.06%). 13C-palmitate-albumin was infused under fed conditions and 13C-palmitate-methyl-beta-cyclodextrin was infused under fasted and fed conditions in 50-kg pigs. Palmitate remained in solution at 4 degrees C in methyl-beta-cyclodextrin, but precipitated at 25-30 degrees C in 2-hydroxypropyl-beta-cyclodextrin. Pigs infused with 13C-palmitate-methyl-beta-cyclodextrin maintained normal body temperature and appetite; those infused with 13C-palmitate-albumin became anorexic and exhibited other negative side effects to albumin. Palmitate oxidation rates under fed conditions were similar using either 13C-palmitate-methyl-beta-cyclodextrin or 13C-palmitate-albumin complexes. Fasting increased 13C-palmitate-methyl-beta-cyclodextrin oxidation by approximately eight-fold. These data suggest that methyl-beta-cyclodextrin may be a suitable substitute for albumin in fatty acid metabolism studies in swine.

The dietary dose responsiveness of conjugated linoleic acid (CLA) addition relative to the fatty acid profile of edible lean tissue was examined in grower pigs treated with or without porcine somatotropin (pST). Gilts and barrows were fed CLA at 0, 0.25, 0.5, 1.0, or 2.0% of diet by weight from 20 to 55 kg BW. Additional pigs were administered (pST) at 0 or 100 microg x kg BW x d(-1) and fed either 0.5 or 2.0% CLA. Animals were fed diets containing 18% CP, 1.2% lysine, and 3.5 Mcal of DE/kg at 110% of ad libitum intake. The fatty acid profile in latissimus dorsi and dorsal s.c. adipose tissue samples was determined by gas chromatography. Dietary CLA replacement of corn oil increased the percentage of total fatty acids as stearic acid, whereas the percentages as oleic and linolenic acids were reduced in lattisimus muscle. Treatment with CLA + pST increased the percentages of linoleic and arachidonic acids while reducing the percentages of palmitic and oleic acids in lattisimus muscle. Dietary CLA increased the percentages of palmitic and stearic acids in s.c. adipose tissue while reducing the percentages of oleic, linoleic, linolenic, and arachidonic acids. The percentage of palmitic acid was reduced in s.c. adipose tissue, whereas linoleic acid was increased with CLA + pST. No synergistic effect was detected between CLA and pST for reducing carcass lipid content in grower pigs. However, pST increased the percentage of polyunsaturated fatty acids in lattisimus muscle and s.c. adipose tissue while reducing the percentages of saturated fatty acids in swine fed CLA.

Somatotropin (ST) administration enhances protein deposition and elicits profound metabolic responses, including hyperinsulinemia. To determine whether the anabolic effect of ST is due to hyperinsulinemia, pair-fed weight-matched growing swine were treated with porcine ST (150 microg x kg body wt(-1) x day(-1)) or diluent for 7 days (n = 6/group, approximately 20 kg). Then pancreatic glucose-amino acid clamps were performed after an overnight fast. The objective was to reproduce the insulin levels of 1) fasted control and ST pigs (basal insulin, 5 microU/ml), 2) fed control pigs (low insulin, 20 microU/ml), and 3) fed ST pigs (high insulin, 50 microU/ml). Amino acid and glucose disposal rates were determined from the infusion rates necessary to maintain preclamp blood levels of these substrates. Whole body nonoxidative leucine disposal (NOLD), leucine appearance (R(a)), and leucine oxidation were determined with primed, continuous infusions of [(13)C]leucine and [(14)C]bicarbonate. ST treatment was associated with higher NOLD and protein balance and lower leucine oxidation and amino acid and glucose disposals. Insulin lowered R(a) and increased leucine oxidation, protein balance, and amino acid and glucose disposals. These effects of insulin were suppressed by ST treatment; however, the protein balance remained higher in ST pigs. The results show that ST treatment inhibits insulin's effects on protein metabolism and indicate that the stimulation of protein deposition by ST treatment is not mediated by insulin. Comparison of the protein metabolic responses to ST treatment during the basal fasting period with those in the fully fed state from a previous study suggests that the mechanism by which ST treatment enhances protein deposition is influenced by feeding status.

Somatotropin (ST) administration enhances protein deposition in well-nourished, growing animals. To determine whether the anabolic effect is due to an increase in protein synthesis or a decrease in proteolysis, pair-fed, weight-matched ( approximately 20 kg) growing swine were treated with porcine ST (150 microg. kg(-1). day(-1), n = 6) or diluent (n = 6) for 7 days. Whole body leucine appearance (R(a)), nonoxidative leucine disposal (NOLD), urea production, and leucine oxidation, as well as tissue protein synthesis (K(s)), were determined in the fed steady state using primed continuous infusions of [(13)C]leucine, [(13)C]bicarbonate, and [(15)N(2)]urea. ST treatment increased the efficiency with which the diet was used for growth. ST treatment also increased plasma insulin-like growth factor I (+100%) and insulin (+125%) concentrations and decreased plasma urea nitrogen concentrations (-53%). ST-treated pigs had lower leucine R(a) (-33%), leucine oxidation (-63%), and urea production (-70%). However, ST treatment altered neither NOLD nor K(s) in the longissimus dorsi, semitendinosus, or gastrocnemius muscles, liver, or jejunum. The results suggest that in the fed state, ST treatment of growing swine increases protein deposition primarily through a suppression of protein degradation and amino acid catabolism rather than a stimulation of protein synthesis.

The ontogeny of the somatotropin/insulin-like growth factor system was examined in well-fed pigs under basal conditions and during a short-term challenge of porcine ST (pST). The study was conducted with two replicates of eight castrate male pigs from 3.8 kg BW (10 d of age) to 92 kg BW (129 d of age). Pigs were reared individually with ad libitum access to milk replacer through 23 d of age. Thereafter, pigs were fed a corn, soybean meal, and dry skim milk diet formulated to exceed nutrient requirements by approximately 30%. Pigs were randomly assigned to receive daily i.m. injections of either 0 (buffer) or 120 microg/kg BW of pST for a duration of 4 d starting at 10, 19, 33, 43, 63, 83, and 125 d of age. Blood was collected via jugular venipuncture on d 0 and 4 of the challenge. Circulating levels of IGF-I were not dramatically affected by age, but levels of IGF-II were low from 10 to 19 d of age and then increased through later stages of growth. Circulating concentrations of IGF binding protein (BP)-3 increased with age (P < .05), but levels of IGFBP-2, a 30-kDa IGFBP, and IGFBP-4 were unchanged (P > .10). The pST challenge reduced plasma urea nitrogen at all ages, but the magnitude of the response was less in younger pigs compared with the maximum response in pigs greater than 30 kg BW (63 d of age). The IGF-I response to the pST challenge also increased from approximately 30% in young pigs to a threefold increase in older pigs. Regardless of age, concentrations of IGF-II were minimally affected by the pST challenge. Circulating levels of IGFBP-3 increased and IGFBP-2 levels decreased in response to the pST challenge, and the magnitude increased with age. The high nutritional status of pigs in the early phases of growth diminished the postnatal changes in IGF-I and IGFBP-2, but not IGF-II or IGFBP-3. Overall, data demonstrate a developmental regulation of the ST/IGF system, with pST challenges altering circulating concentrations of IGF-I, IGFBP-3, and IGFBP-2 coincident with changes in amino acid metabolism.

Growing (35 kg body weight) and finishing (85 kg body weight) swine challenged with endotoxin (Escherichia coli O55:B5) at a dose of either 2 or 20 microg/kg produced tumor necrosis factor (TNF)alpha in a dose-response relationship as measured by bioassay. Peak TNFalpha plasma levels were observed 1-2 hr post-challenge, returning to basal values 4 hr post-challenge. However, both an enzyme-linked immunosorbent assay specific for swine TNFalpha and total human TNFalpha demonstrated no dose-response relationship; peak plasma levels of immunoreactive TNFalpha were also observed 1-2 hr post-challenge. Maximal plasma interleukin-6 levels occurred 1-2 hr post-challenge and remained elevated through 8 hr post-challenge; there was no effect of lipopolysaccharide dose or metabolic status. Although the metabolic status of the animals also affected glucose levels, with growing animals exhibiting greater sensitivity compared with finishing animals, endotoxin-induced decreases in blood glucose levels were primarily dose-dependent. In contrast, changes in plasma urea nitrogen and free fatty acid (FFA) levels were strictly related to the metabolic status. Urea nitrogen levels were unchanged in growing swine, whereas they were increased in finishing swine and remained elevated 24 hr post-challenge. FFA levels in growing and finishing swine increased 3-6 hr post-challenge. FFA levels returned to basal values for finishing swine 24 hr post challenge, but in growing swine remained elevated 24 hr post-challenge. Plasma aspartate transaminase levels were increased through 24 hr post-challenge; animals given a dose of 20 microg/kg exhibited the greatest increase. Similarly, swine challenged with a dose of 20 microg/kg also exhibited the greatest increase in levels of conjugated bilirubin; there was no effect on unconjugated (free) bilirubin. These results demonstrate that endotoxin challenge of swine result in a pattern of changes that are dependent on both the dose of endotoxin used and the metabolic status of the animal examined.

Growth rate and body composition of livestock can be optimized to meet consumer needs for a leaner product and to improve the efficiency of meat-animal production. Optimization strategies have traditionally focused on genetic selection and cost-effective ration formulation to achieve the genetic potential. Advances in understanding the mechanisms of growth and its control have led to additional opportunities for its manipulation. These include nutritional manipulation,the use of growth promotants, and, more recently, the ability to change the genetic potential through genetic engineering. Selection of appropriate candidate genes for manipulation depends on understanding the mechanisms underlying differentiation and growth of embryonic muscle cells. Recent advances in genetic engineering techniques, including gene therapy and germline transgenesis, will likely hasten the genetic progress toward a leaner carcass in domestic livestock. Such strategies may prove to be more beneficial then the controlled enhancement of somatotropin expression.

Two experiments were conducted with cross-bred barrows to determine the effect of somatotropin administration on liver enzyme activities. In the first experiment, pigs growing from 26 to 55 kg body weight were given two doses of pituitary porcine somatotropin (pST; 0 and 100 micrograms per kg body weight) and three levels of dietary energy (60, 80 and 100% of free choice intake). In the second experiment, pigs growing from 30 to 60 kg body weight were given two doses of recombinant porcine somatotropin (rpST; 0 and 100 micrograms per kg body weight) and five levels of dietary crude protein (110, 150, 190, 230 and 270 g crude protein/kg diet). Liver arginase (ARG, EC 3.5.3.1) and aspartate aminotransferase (AAT, EC 2.6.1.1) activities were then determined in organ samples taken at slaughter time. Dietary energy did not change liver ARG. Activities of both ARG and AAT increased as dietary crude protein increased. Both pST and rpST decreased ARG, AAT and serum utrea nitrogen. There was a lack of interaction between rpST therapy and dietary protein on either ARG or AAT activities, suggesting that set nutritional states are not required for expression of pST effects.

We conducted two experiments to determine the efficacy of exogenous porcine somatotropin (pST) on enhancing performance during an early phase of growth (10 kg initial BW) when pigs are already growing efficiently and have high rates of lean deposition and low rates of lipid deposition. In Exp. 1, performance was measured on 45 barrows that received one of five daily doses (0, 50, 100, 150 and 200 microg/kg BW) of recombinant pST. In Exp. 2, 27 barrows were used in a slaughter-balance study in which two groups received daily either buffer (control) or 120 microg/kg BW of pST and the third group was slaughtered for initial body composition. In both experiments, pigs received daily i.m. injections of their respective dose for 20 d. The diet was fed for ad libitum consumption and calculated to contain 3.5 Mcal DE/kg, 22.3% CP, and 1.5% lysine. Administration of pST failed to alter overall growth rate or efficiency of gain in either experiment. However, in Exp. 2 pigs treated with pST had increased deposition rates of protein and water but reduced lipid deposition rates. Furthermore, pST treatment resulted in characteristic reductions in plasma urea nitrogen and elevations in glucose and NEFA. Plasma concentrations of insulin and IGF-I were also increased, but pST reduced IGF-II and IGF binding protein-2. Overall, the data demonstrated that very young pigs respond to pST with enhanced lean tissue accretion and metabolic changes, but the response is attenuated compared with previous studies in older growing pigs.

Barrows were restrictively fed starting at 20 kg BW to determine the effects of endotoxin on growth performance of control and somatotropin-treated pigs. The following treatments were used: 1) daily i.m. vehicle injection until 55 kg BW; 2) daily i.m. injections of 100 micrograms of recombinant porcine somatotropin (pST)/kg BW, until 55 kg; 3) i.v. saline injections for 7 d consecutively starting at 60 kg BW; 4) i.v. injections of 1 microgram of bacterial lipopolysaccharide (LPS)/kg BW for 7 d starting at 60 kg BW; and 5) the combined LPS+pST treatment, with pST injections from 20 kg through the 7 d of LPS treatment. Pigs evaluated for LPS effects were fed to 60 kg anticipating a weight loss. Pigs were bled at 0800 and 1100 at 55 kg and on d 7 of LPS treatment. Rectal temperatures were taken on d 7. Treatment with pST increased ADG by 13 to 20% and improved feed:gain by 17 to 23% before LPS treatment. During the 7 d of LPS injections, ADG and feed:gain did not differ, although feed efficiency was impaired and variable. Rectal temperatures at 1100 were progressively increased: control < LPS < LPS-pST (P < .01). Protein accretion was improved 27% by pST treatment, and lipid accretion was decreased 45% before LPS. Lipid stores decreased (P < .01) after LPS treatment in the pST-treated pigs. Lipopolysaccharide treatment and(or) decreased feed intake reduced the hyperinsulinemia and hyperglycemia (P < .01) associated with pST treatment. These results indicate that LPS induced a simulated septicemia and that the effects were not negated by pST treatment. The observed hyperthermia was additive, possibly due to increased lean body mass induced by pST combined with the pyrogenic effect of LPS.

Objective: To determine whether recombinant porcine somatotropin (PST) or chromium picolinate (CrP) affected cytokine production and metabolism in swine after endotoxin challenge exposure., Animals: 20 Poland China X Landrace pigs, 5/group., Procedure: Pigs were given CrP-supplemented feed at body weight of 20 kg; PST treatment began at 60 kg, and both treatments continued through body weight of 90 kg. At 90 kg, pigs were challenge exposed with 20 micrograms of lipopolysaccharide (LPS)/kg of body weight. Blood samples were obtained at various times through 24 hours after LPS challenge exposure., Results: In all pigs not given PST, glucose concentration decreased 2 to 4 hours after LPS. In PST-treated pigs, blood glucose concentration was decreased at 6 to 8 hours after LPS. Plasma insulin concentration paralleled changes in glucose concentration. Nonesterified fatty acid concentration was high 2 to 24 hours after LPS in pigs not given PST and at 6 to 24 h in PST-treated pigs. Plasma urea nitrogen concentration was high at 6 to 24 hours after LPS in pigs not given PST. The urea nitrogen values in PST-treated pigs were lower at all times. Serum aspartate transaminase activity was high 6 to 24 hours after LPS in pigs not given PST, whereas PST treatment prevented the increase in this enzyme activity. In untreated (PST) pigs, plasma bilirubin (total and direct) concentrations were high 4 to 8 hours after LPS and returned to normal at 24 hours. The PST- and CrP-treated pigs maintained normal plasma bilirubin concentrations. Interleukin 6 activity was unaffected by CrP and PST treatments. Treatment with CrP and PST decreased the tumor necrosis factor alpha response to LPS, compared with that in control pigs., Conclusions: PST, and to a lesser extent CrP, provide protection against the adverse metabolic effects of LPS-induced septic shock.

Chromium (Cr) and somatotropin have been shown to increase lean body mass in pigs but by independent mechanisms. Somatotropin and Cr also affect blood glucose, lipids, and tissue trace metal concentrations. Twenty-four castrated male pigs were divided into four groups: 1) control basal diet; 2) basal diet + 300 micrograms of Cr/kg of diet as Cr picolinate; 3) basal diet + pituitary porcine somatotropin (ppST; 100 micrograms/kg live weight injected daily); and 4) basal diet + Cr + ppST. Pigs were fed the diets from 30 to 60 kg body weight and then killed. Supplemental Cr led to increased total Cr in kidney (1.1 vs 2.3 micrograms) and liver (5.9 vs 8.8 micrograms) but not in the heart independent of ppST treatment. Chromium concentrations in longissimus muscle were less than 1.5 ng/g in all samples, and any increases due to supplemental Cr were not detected. Somatotropin treatment led to decreased hepatic Cr, Cu, Fe, and Zn concentrations and increased total renal Cu, Fe, and Zn. These data demonstrate that supplemental Cr causes increased tissue Cr in the liver and kidney but not in the heart or muscle in control and somatotropin treated pigs. Somatotropin treatment caused decreased kidney and liver Cr concentrations that were offset by increased tissue weights. Somatotropin effects on tissue Cr, Cu, Zn, and Fe were variable and difficult to evaluate due in part to growth hormone-induced changes in organ weights.

The objective of this review is to summarize data on the interrelationships that exist between nutrition, the endocrine system and their modulation of plasma tumor necrosis factor-alpha responses to endotoxin in cattle. During stress, intake of nutrients often is compromised and a percentage of available nutrients are diverted away from growth processes to stabilize other physiological processes of a higher survival priority. Management practices that minimize the magnitude and duration of disease stress will aid in speeding the return to homeostatic equilibrium. However, the shift away from growth during stress is almost inevitable as a mechanism to survive. Some degree of control and management of the metabolic cost of disease stress involves understanding the integration of nutritional, endocrine and immune signals by cells and working with the natural homeostatic processes. Endocrine hormones and immune system cytokine signals participate in redirecting nutrient use during disease stress. In an intricate interplay, hormones and cytokines regulate, modify and modulate each other's production and tissue interactions to alter metabolic priorities. Levels of dietary protein and energy intake affect patterns of hormones and cytokines in the blood after endotoxin challenge and further modulate the biological actions of many of these regulatory effectors. In vivo, administration of growth hormone to young calves has significant effects to decrease the many specific physiological responses to endotoxemia. Many aspects of nutrition can attenuate or facilitate this effect.

Swine were divided into four groups of 11 animals at 40 kg body wt. Swine within a group were given a single porcine somatotropin (pST) injection (200 micrograms/kg) or buffer at 0800. Blood, liver (L), latissimus dorsi (LD), semitendinosus (STS), vastus lateralis (VL), dorsal subcutaneous (SQ), and perirenal (PR) adipose tissues were sampled at 0, 1, 2, 4, 8, 12, 16, and 24 h postinjection. Blood urea nitrogen was depressed by 16 h. Insulin was elevated by approximately 350% at 8 h. Lipogenic enzyme activities in adipose tissues were not affected by pST treatment. Insulin-like growth factor I (IGF-I) mRNA levels increased rapidly in SQ, PR, and L to a single pST administration, whereas they increased only slightly in VL. IGF-I mRNA concentrations in LD and STS were unaffected by pST treatment. IGF-I protein content of tissues changed little during the first 24 h postinjection. These data suggest that individual tissues differ in timing and degree of response to pST. Conflicting results reported after pST treatment could, in part, be due to tissue selection for sampling or sample timing.

This experiment was conducted to establish the influence of porcine somatotropin on tissue distribution and deposition rates of amino acids in growing pigs. Barrows were treated daily with buffer or porcine somatotropin (100 micrograms/kg body wt) when they weighed between 30 and 64 kg (eight pigs/group). Pigs were restrictively fed so that the average food intake was 1.86 kg/d. The corn-soybean meal-skim milk-based diet contained 18% crude protein and 1.2% lysine, and was designed to meet muscle amino acid ratio profile with respect to lysine as the first limiting amino acid for growth. Tissue levels of eighteen amino acids were determined on lyophilized samples that were appropriately hydrolyzed and analyzed by HPLC. The concentrations (mg/g dry wt) of all amino acids were greater in carcass, skin, head and empty body of porcine somatotropin-treated pigs; amino acid concentration in viscera was not influenced by porcine somatotropin. However, when the concentration of each amino acid was expressed on a per unit protein basis, the amino acid profiles of control and porcine somatotropin-treated pigs were quite similar. The average deposition rate of each amino acid was increased approximately 67% by porcine somatotropin. When the deposition of each amino acid was calculated in relation to lysine, however, the pattern of amino acid utilization for growth was similar for control and porcine somatotropin-treated pigs; exceptions were arginine, glycine and tryptophan. The ratio of indispensable to dispensable amino acids that were deposited was also similar for control and porcine somatotropin-treated pigs. These data indicate that the synthesis rate of individual proteins can be influenced by porcine somatotropin, but the balance of amino acids remains largely unaffected, suggesting that the changes in protein and amino acid metabolism elicited by porcine somatotropin are consistent with normal growth processes.

This research was conducted to evaluate the characteristics of muscle fiber growth and the effects of porcine somatotropin (pST; 100 micrograms.kg-1 BW.d-1) administration on the morphology of 12 muscles located in different regions of the body in barrows growing from 20 to 90 kg BW. In the course of the growth of control pigs, the percentage distribution of beta R fibers did not show any changes in all 12 muscles, whereas the percentage of alpha R and alpha W fibers changed in different patterns in different muscles. The administration of pST had no effect on fiber type distribution. The cross-sectional area of alpha W fibers was the largest of the three fiber types, and beta R and alpha R fibers were of similar size in all muscles. All fiber types in all muscles increased in cross-sectional area by an average of 120% from 20 to 60 kg BW. After 60 kg BW, the growth of alpha W fibers in seven (early maturing) muscles and alpha R fibers in one muscle out of the 12 muscles was not apparent. The increase of their cross-sectional area was an average of 12%, but the area of the other muscle fibers continued to increase by an average of 38% until 90 kg BW. The administration of pST increased the area of alpha W fibers in four out of seven of these early-maturing muscles by an average of 25%, suggesting some possible relationships between pST effects and the rate of muscle fiber maturation. Most of the muscles that responded to pST treatment were located in hindlimb region.

In a 2 x 2 treatment array (n = 4 pigs/treatment), the effects of feed intake (ad libitum vs. restricted to 60% ad libitum) and the daily administration of excipient buffer or porcine pituitary-derived growth hormone (GH) at a dose of 100 micrograms/kg body weight per day on serum GH profile and human growth hormone-releasing factor (hGRF) response were examined in barrows weighing 55 kg. Feed intake treatment was implemented from 25 to 55 kg live weight. Buffer or GH treatment was implemented for 10 d before sampling. After GH treatment, the integrated serum GH concentration area was 25% greater in barrows fed restrictively. Data are consistent with the suggestion that GH dose to improve the efficiency of lean tissue deposition be adjusted according to feeding regimen. The serum GH response to hGRF was also altered by level of feed intake. The ad libitum feeding of buffer-treated animals resulted in a monophasic serum GH response to hGRF, whereas barrows fed restrictively had a biphasic response to hGRF. Together, these data suggest that feed intake pattern alters GH secretion and as such could influence the practical implementation of somatotropin as a metabolism modifier in swine.

The effect of dietary chromium picolinate (CrP) and recombinant porcine growth hormone, somatotropin (rPST) administration on growth performance and cytokine production in Landrace-Poland China gilts was determined using a 2 by 2 treatment array. Treatments were: (1) control (basal diet), (2) CrP-supplemented diet (basal diet + 300 micrograms Cr3+/kg diet as CrP), (3) rPST (100 pg/kg body weight/day), and (4) rPST+CrP. CrP-supplemented diets were fed beginning at 20 kg body weight through 90 kg. Administration of rPST was begun at 60 kg weight and continued through 90 kg. All rPST treated pigs demonstrated improvements in growth performance versus controls. Pigs given CrP-supplemented diets showed no differences in growth performance. At 90 kg, pigs were challenged with endotoxin (lipopolysaccharide, 0.2 microgram/kg i.v.). Blood samples were collected at 0, 1, and 3 h postchallenge. Plasma IL-6 levels increased from 23 U/ml at time 0 to 1,927 U/ml at 3 h for control swine. Swine from the CrP treatment group had IL-6 levels of 8,130 U/ml at 3 h post-LPS. There were no differences in plasma IL-6 from pigs in the rPST and rPST+CrP treatment groups compared to the controls. Endotoxin challenge had no effect on either blood glucose levels or induction of TNF-alpha in any treatment group. PBMC from CrP-treated animals produced more IL-2 than peripheral blood mononuclear cells from all other groups.

Diabetes alters the level of insulin-like growth factor I (IGF-I) mRNA in tissues of postnatal animals, but the impact of maternal diabetes or gestational diabetes on IGF-I mRNA abundance in fetal tissues has not been examined. Pregnant pigs were injected with either buffer or alloxan (50 mg/kg) at day 75 of gestation to induce diabetes. Fetal tissue samples were collected at day 105 of gestation, and IGF-I mRNA abundance (densitometric units/10 micrograms total RNA) were estimated by specific ribonuclease protection assay. Fetal glucose and IGF-I concentrations were increased 166 and 34%, respectively, by maternal diabetes. Maternal diabetes induced an increase in abundance of IGF-I mRNA in fetal skeletal muscle, liver, heart, kidney, and placenta. IGF-I mRNA levels were depressed by maternal diabetes in fetal adipose tissue and brain compared with the respective tissues from fetuses of control pigs. These data indicate that circulating levels of IGF-I and the steady-state levels of IGF-I mRNA in fetal tissues can respond to the metabolic and endocrine alterations occurring during maternal diabetes. The large variation in expression and degree of response among fetal tissues indicates that the fetus experiences tissue-specific regulation of IGF-I expression during development.

The level of protein in the diet both before and during treatment with beta-adrenergic agonist (BAA) was investigated with regard to its effect on growth performance and carcass characteristics of pigs. A total of 76 pigs were divided into two groups and given ad libitum access to diets containing either 12 or 18% crude protein (CP) during growth from 15 to 60 kg. At 60 kg, six pigs from each group were slaughtered and carcass composition was determined. For the test period (growth from 60 to 90 kg) the remainder of the pigs were divided into eight groups of eight pigs each. Half of the pigs from each of the two dietary pretreatment groups were switched to the other diet and half remained on the same diet. Of the four dietary groups, half were fed 0 mg/kg (controls) or 1 mg/kg of BRL 47672. During the test period, all pigs were fed at 90% of their calculated ad libitum DE intake. All pigs were slaughtered at 90 kg and carcass composition was determined. Addition of BRL 47672 to the diet resulted in an overall improvement (P < .05) in daily gain (.72 vs .64 kg) and gain/feed (.28 vs .26); the greatest improvement occurred with pigs fed the 18% CP diet (24 and 14% for daily gain and gain/feed, respectively). Pigs that had received BRL 47672 also had 12% less backfat, 10% less carcass lipid, 16% larger longissimus muscle area, and 5% more carcass protein (P < .05 for each), and the greatest changes occurred in pigs fed the 18% CP diet (-26, -16, +21, and +10%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Sixty crossbred barrows (average 30 kg) were used in a 5 x 2 factorial treatment array to examine interactions between dietary protein concentration (11, 15, 19, 23, or 27% CP) and recombinant porcine somatotropin (rpST: 0, excipient buffer vs 100 micrograms.kg-1.d-1) for 42 d on muscle fiber morphology and meat tenderness. Diets were isocaloric (3.8 Mcal of DE/kg) and of equal lysine (4.9 g/Mcal of DE) achieved by diluting soybean meal with cornstarch and by addition of crystalline lysine. Dosage of rpST and feed intake (80% of predicted ad libitum) were adjusted weekly. Four muscles (longissimus = LM; semimembranosus = SM; semitendinosus = ST; triceps brachii = TB) were evaluated. Percentages of muscle fiber types (beta R, alpha R, alpha W) for the LM, SM, and TB were not influenced by rpST treatment. More alpha R and fewer alpha W fibers were found in the ST muscle of rpST-treated pigs. No interactions were observed between rpST treatment and dietary protein for muscle fiber type distribution. Dietary protein had no consistent influence on the distribution of muscle fiber types in all four muscles. Area of fibers generally increased in rpST-treated pigs compared with controls when diets contained 19% or more CP. The LM shear force was increased (13%) by rpST treatment for chops frozen after 5 d of storage in the cooler, but not in those chops frozen within 1.5 h postmortem. Dietary protein had a variable influence on tenderness. These data indicate that muscle fiber growth (hypertrophy) in pigs is positively influenced by rpST treatment. Marginal dietary protein intake reduces muscle fiber growth responses to rpST.

A study was conducted to determine the feasibility of using differences in the natural abundance of dietary 13C as a means of in vivo labeling. Four female pigs were fed a C3 plant diet (barley, soybean meal and alfalfa) and four were fed a C4 plant diet (corn and corn gluten meal). The pigs were continually fed the diets from 8 wks of age to maturity and through pregnancy until they had themselves produced offspring. The resulting piglets were sacrificed at various time intervals (0 to 165 days) after switching either the piglets or their mothers' to the opposite diet. Changes in the delta 13C levels in samples of milk and tissues following the diet change were monitored by isotope ratio mass spectrometry. The differences in the delta 13C content of the two diets was 12.9 parts per mil (/1000). After piglets born to a sow fed the C3 diet were switched at one day of age to a surrogate sow fed the C4 diet, tissue delta 13C levels of the piglets were nearly identical to the diet of the surrogate sow by 11 days while those switched from C4 to C3 grew more slowly and differed from the diet by 2-5/1000. When the mothers diet was switched, 15-20 days later the delta 13C in the milk had changed by only 2-3/1000, indicating that the body rather than the diet was the primary source of carbon in the milk. At 28 days after the piglets diet was switched at weaning, the tissue delta 13C had changed by 8.4/1000 (C4 to C3) and 2.9/1000 (C3 to C4). The delta 13C level in the liver changed more rapidly than in the muscle or fat and the rate of change was also influenced by the size and growth rate of the pig.

Twenty-four castrated male pigs were used in a 2 x 2 treatment array to determine the main effects of and interactions between dietary chromium supplementation and pituitary porcine somatotropin (ppST) administration on growth performance and serum hormone and metabolite concentrations. The treatments were 1) control (basal diet); 2) chromium (basal diet+300 micrograms/kg diet added trivalent chromium as chromium picolinate); 3) ppST (100 micrograms/(kg body wt.d); and 4) chromium+ppST. Treatments were administered when pigs weighed between 30 and 60 kg. Blood was collected when pigs weighted 45 and 60 kg. All pigs treated with ppST exhibited improvements in growth performance (P < 0.05). Pigs given chromium showed no improvements in growth rate, feed efficiency or composition of gain. Measurements at 60 kg body weight revealed that ppST increased the cholesterol:HDL cholesterol ratio (P < 0.05). Chromium lowered serum insulin and glucose concentrations relative to controls (P < 0.05) and normalized the increase in glucose and insulin resulting from ppST treatment. No ppST x chromium interactions were noted, suggesting these changes in glucose and insulin metabolism are exerted through different mechanisms. These results indicate that chromium does not affect growth performance of young growing pigs. Chromium does normalize altered hormone and metabolite concentrations resulting from ppST treatment.

Three groups of eight gilts weighing 20, 40, or 60 kg were fitted with indwelling venous catheters to determine daily integrated circulating levels (DICL, serum concentration above baseline x time) of insulin, growth hormone (GH), glucagon, glucose, urea, and nonesterified fatty acids (NEFA) in response to acute challenge with porcine pituitary GH (pGH). Pigs were fed a common diet containing 18% CP and 3.5 Mcal of DE/kg between 0800 and 1200 (85% of ad libitum). Blood and urine were collected at 2- or 4-h intervals for 4 d. On d 2, 3, and 4, four pigs in each group were injected i.m. at 0800 with pGH (.1 mg/kg) and four pigs (controls) were injected with buffer. In control pigs DICL of GH was 20.4, 14.1, and 10.2 ng pGH.h.mL-1 in 20-, 40-, and 60-kg pigs, respectively. The DICL of GH in pGH-treated pigs was 4.2-, 7.0-, and 10.7-fold greater in 20-, 40-, and 60-kg pigs, respectively, than in controls. The DICL of insulin in control pigs was 7.9, 9.7, and 9.4 ng.h.mL-1 and was increased (P < .001) in pGH-treated pigs by 118, 213, and 276% in 20-, 40-, and 60-kg pigs, respectively. Although serum levels of glucose were increased (P < .001) by pGH treatment, the acute elevation observed in 60-kg pigs was more consistent relative to 20- and 40-kg pigs. In contrast, the acute reduction in blood urea upon pGH injection was more apparent in 20-kg gilts.(ABSTRACT TRUNCATED AT 250 WORDS)

Thirty-two crossbred barrows were used to determine the effects of frequency of administration of equivalent total dosages of recombinant porcine somatotropin (rpST) on growth performance, tissue accretion rates, and hormone and metabolite status of pigs. Treatments were control (buffer-injected daily), 60 micrograms/kg BW daily (4 injections/4 d), 120 micrograms/kg BW injected every other day (2 injections/4 d), or 240 micrograms/kg BW given every 4th d (1 injection/4 d). Treatments were initiated at 35 BW and continued until each pig had consumed a total of 440 Mcal of DE intake. Pigs were fed a diet that contained 16% CP, 1.2% lysine, and 3.5 Mcal of DE/kg at 85% of calculated ad libitum intake. Feed intake and rpST dose were adjusted at 8-d intervals. The 240 micrograms/kg BW treatment did not decrease appetite beyond the 15% restriction already imposed in the experimental design. Treatment groups responded to rpST in a frequency-dependent manner. Average daily gain was improved by 10, 23, and 36%, respectively, as injection frequency was increased from 1/4 to 2/4 to 4/4 d. Muscle weights were increased uniformly (15% on average) on a BW basis by all rpST treatments. Carcass (21, 42, and 63%), visceral (43, 65, and 112%), and empty body (22, 43, and 65%) protein accretion rates were increased by rpST treatment in a frequency-dependent fashion, respectively. Lipid accretion also was reduced in carcass and empty body (31% on average) by all rpST injection schemes relative to controls; however, visceral lipid accretion was increased by 59% by rpST. Protein utilization efficiency increased linearly by 24, 45, and 65% as the frequency of injection of rpST was increased from 1/4 to 2/4 to 4/4 d. Hormones and metabolites exhibited frequency-related profiles as well. These results suggest that frequency of administration greatly influences the magnitude of responsiveness to rpST and that optimal benefit would be realized by a delivery system that mimicked a daily surge, at minimum, of rpST.

The effect of ractopamine, a beta-adrenergic agonist, on growth, nutrient utilization, and carcass composition was studied in pigs fed either 18% CP, 12% CP, or 18% CP restricted (RES = 67% of ad libitum) diets. The 18 and 12% CP diets provided 3.52 and 3.68 Mcal of DE/kg, respectively. All pigs were fed a low-protein (12% CP) diet during pretreatment growth from 15 to 60 kg. Ractopamine at 20 or 30 ppm (30 ppm for RES pigs) in the diet was fed from 60 kg live BW until slaughter at 105 kg (9 pigs/treatment). No ractopamine treatment effect (P greater than .05) was observed for either daily gain or gain/feed, although gain/feed was improved by 8% in both of the ad libitum groups. Ractopamine treatment resulted (P less than .01) in an overall reduction of carcass lipid by 8%, an increase of carcass protein by 5%, and a 21% improvement in the efficiency of protein utilization; the greatest changes occurred in the pigs fed the 12% CP diet (-17%, +11%, and +32%, respectively). The ad libitum daily feed intake was 15% less for pigs fed the 12% CP diet than for those fed the 18% CP diet (P less than .01), and there was a 10% reduction in intake of both diets with the addition of ractopamine (P less than .05). Both carcass lipid and protein deposition seemed to be closely related to energy intake (P less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

The present study was conducted to determine the effects of different dietary protein levels and recombinant porcine somatotropin (rpST) administration on deposition rates of protein, fat, water, ash, and collagen in pigs. Ten groups of six barrows (30 kg BW) were restrictively fed (80% of ad libitum) one of five diets containing 11, 15, 19, 23, or 27% CP. Diets were isoenergetic and all contained equivalent amounts of lysine. Thirty barrows were treated daily with rpST (100 micrograms/kg) by i.m. injection; remaining pigs were treated with diluent for 42 d. At all levels of dietary protein intake, carcass and empty body accretion rates of protein, water, and ash were greater in rpST-treated pigs than in respective controls. The magnitude of change elicited by rpST was lowest in pigs consuming 11% CP. Administration of rpST resulted in a 34% decrease in the accretion rate of fat; increasing protein intake resulted in a linear decrease in fat accretion in control and rpST-treated pigs. Accretion rates of protein, water, ash, and fat were increased in viscera of rpST-treated pigs compared with respective controls; rates of visceral protein and water accretion were increased as dietary protein was increased, whereas deposition of fat was decreased in control and rpST-treated pigs. Administration of rpST resulted in an overall 66% increase in the utilization efficiency of dietary protein for empty body protein deposition. Protein intake had minimal effect on the concentration of collagen in the carcass; however, rpST treatment increased concentrations of total and soluble collagen by 30 and 33%, respectively. Recombinant pST had little influence on collagen crosslinking or maturation. Deposition rate of carcass collagen was increased 63% in rpST-treated pigs compared with respective controls.

Thirty-six barrows were used in a 2 X 3 factorial treatment array to determine the effects of time of injection (0800 [AM] or 1800 [PM]) of recombinant porcine somatotropin (rpST) (0, 50, or 100 micrograms.kg BW.d-1 adjusted weekly) relative to time of feeding on growth performance, carcass composition, serum hormones and metabolites, and muscle RNA, DNA, and protein. Pigs were fed at 85% of ad libitum and allowed access to feed between 0800 and 1200. Treatments were initiated at 38 kg and continued until each pig consumed an average of 7.5 Mcal of DE/d. There was no significant effect of injection time for any measure of growth performance or composition of gain even though rpST treatment improved most criteria evaluated. Treatment with rpST increased ADG by 30%, improved feed:gain by 23%, reduced lipid accretion by 46%, increased protein accretion by 69%, and increased loin eye area (LEA) by 26%. Time of injection also had no effect on serum hormones or metabolites, except for nonesterified fatty acids (NEFA), which were 20% higher in the AM-injected animals. Treatment with rpST increased (P less than .05) RNA concentration (21%) and RNA/DNA (17%) in longissimus dorsi (LD) muscle. In semimembranosus (SM) muscle, however, rpST administration resulted in an increased (P less than .05) DNA concentration (10%) and a decreased DM content (4%). These results suggest that rpST influences growth differently in these two muscles. We conclude that time of rpST administration (AM vs PM) has no effect on its metabolic properties and, therefore, no effect on growth performance in the pig.

Twenty-four barrows were used to investigate the effects of exogenous porcine somatotropin (pST) administration (0 and 100 micrograms.kg-1.d-1) between 30 and 60 kg on longissimus muscle morphology and meat tenderness of pigs grown to 90 kg. Administration of pST was by daily i.m. injection. Pigs were fed a fortified diet in restricted amounts between 30 and 60 kg and had ad libitum access to this diet from 60 to 90 kg. Excipient pigs had fewer alpha R fibers and more alpha W fibers than pST-treated pigs (P less than .05). Administration of pST increased (P less than .05) muscle fiber area for all three fiber types at both the 60 kg (34%) and 90 kg (29%) slaughter weights. Furthermore, pST administration increased shear-force (30% at 60 kg; 19% at 90 kg) of the longissimus muscle, indicating that pST administration reduced meat tenderness. All the pST-treated pigs exhibited the "giant fiber syndrome" and a high proportion (62%) of pST-treated pigs exhibited pale, soft, exudative muscle. Whether the giant fiber anomaly resulted from increased muscle protein accretion rate or fiber degeneration is unknown. Results indicated that the stimulatory effects of pST on muscle growth are sustained following cessation of hormone treatment. However, the incidence of pale, soft, exudative muscle in 62% of the pST-treated pigs indicates that pST potentially has undesirable side effects.

The influence of dietary protein and recombinant porcine somatotropin (rpST) administration on growth and body composition was investigated in barrows. Ten groups of six pigs starting at 30 kg were restrictively fed (approximately 80% of ad libitum) one of five diets containing 11, 15, 19, 23 or 27% protein. Diets contained skim milk (12%). Soybean meal diluted with cornstarch was used as the supplemental source of dietary protein. Diets were isocaloric (3.8 Mcal DE/kg) and all contained the same amount of lysine (18 to 20 g/kg). Thirty pigs were treated daily with rpST (100 micrograms/kg) by i.m. injection; the remaining pigs were treated with sterile diluent (control) for 42 d. Growth rate was greater in rpST-treated pigs at all levels of protein intake; however, the magnitude of the response to rpST treatment was lowest among pigs fed the diet containing 11% protein. Feed:gain ratio, backfat depth and carcass fat content were decreased in rpST-treated pigs compared to respective controls. Additionally, the concentration of carcass fat decreased concomitantly with an increase in dietary protein intake. Concentration of carcass protein increased linearly as dietary protein increased in control and rpST-treated pigs. In contrast, treatment with rpST was associated with an increased visceral mass; the concentration of protein and fat in the viscera was influenced by protein intake but not by rpST. These results, characterized by few treatment interactions, suggest that when energy intake is kept constant and appropriately fed pigs serve as controls, dietary protein and rpST influence growth and body composition by independent mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

Experiments were conducted with male broiler breeder chickens to determine the metabolic effects of two levels of dietary crude protein fed during a protein-reversal regimen on subsequent responses to a beta-adrenergic agonist (isoproterenol) in vitro. Day-old chickens were fed diets containing either 12 or 20% crude protein until 14 d of age and then switched to the opposite diet until 28 d. In experiment 1, chickens were killed at 28 d, and in experiment 2, at intervals following the switch at 14 d. In vitro lipogenesis and lipolysis were determined. The hepatic enzymes isocitrate dehydrogenase, malic enzyme and fatty acid synthetase were determined during the 14 to 28 d of age growth period. Both in vitro lipogenesis and lipolysis were greater at 28 d when chickens were fed the 12% rather than the 20% protein diet. Neither 0 to 14 d of age dietary treatment influenced 28-d metabolic parameters. In contrast, the 12% protein diet during the first 14-d period depressed body weight (160 g vs. 320 g; p less than 0.05) and weight gain during the 14 to 28 d of age period regardless of dietary crude protein levels (508 g vs. 626 g; p less than 0.05). Lipogenesis and lipolysis were at their highest points 4 d following the dietary switch. Isoproterenol decreased in vitro lipogenesis 70% in all dietary treatment groups. Stimulated lipolysis was not affected by nutritional status and was twice the unstimulated rate.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of ractopamine, a phenethanolamine beta-adrenergic agonist, on growth, nutrient utilization and carcass composition was studied in two lines of pigs that were fed high (24%) or low (12%) protein diets. Of the two lines of pigs that had been selected for seven generations for rapid lean growth when fed either the higher (HS line) or low (LS line) protein diet, the HS line tended to exhibit a leaner carcass when fed either diet. Ractopamine, at 20 ppm in the diet, was fed from 60 kg live body weight until slaughter at 90 kg. When compared with their respective line-diet control group, the greatest response to ractopamine treatment was observed in the LS-12 group; at 90 kg, that group had 31% less carcass lipid (P less than .05) and 17% more carcass protein (P less than .05). Considering the change that took place only between 60 and 90 kg live body weight, this translated into 57% less lipid and 59% more protein deposited in the carcasses with ractopamine treatment. This group also was 73% more efficient (P less than .05) in converting dietary protein to carcass protein but 39% less efficient (P less than .05) in energy utilization. Response to ractopamine treatment was least by the LS-24 group, followed by the HS-12 and HS-24 groups. A line x diet x treatment interaction (P less than .05) was noted for whole-carcass lipid, backfat, longissimus muscle area and efficiency of protein utilization.(ABSTRACT TRUNCATED AT 250 WORDS)

Chickens were fed on diets containing either 12.8 MJ, 150 g crude protein (nitrogen x 6.25)/kg or 12.8 MJ, 200 g crude protein/kg to determine differences in metabolism. The diet containing 12.8 MJ, 150 g crude protein/kg contained either 8 or 12 g lysine/kg. Treatment variables examined in vitro were lipogenesis, glucose production and hepatic enzyme activities to compare metabolism in chicks fed on a low-protein, lysine-supplemented diet and a diet formulated to contain the required amount of lysine from intact protein. Growth was similar in chicks fed on diets containing either 12.8 MJ, 154 g crude protein with 12 g lysine/kg or 12.8 MJ, 200 g crude protein/kg. Net glucose production was greater (P less than 0.05) in liver explants from chickens fed on diets containing either 12.8 MJ, 154 g crude protein with 12 g lysine/kg or 12.8 MJ, 200 g crude protein/kg than in explants from chickens fed on 12.8 MJ, 150 g crude protein with 8 g lysine/kg. Pyruvate use for glucose production was greater (P less than 0.05) in chickens fed on a diet containing 12.8 MJ, 150 g crude protein with 8 g lysine/kg. The findings from the present study suggest that crystalline and 'natural' lysine additions to chick diets may influence metabolism differently.

Twelve 36-kg pigs were given either 100 micrograms/kg porcine pituitary growth hormone (pGH) or placebo injections daily for 33 days. Serum was obtained weekly for analysis of minerals and vitamin D metabolites. On day 34, the pigs were sacrificed and renal and duodenal tissue were obtained for analysis of vitamin D receptor content (VDR). Animals treated with pGH grew faster and had a higher rate of bone accretion than did control animals. Serum concentrations of 1,25-dihydroxyvitamin D (1,25-(OH)2D) were significantly higher in pGH-treated pigs than in control pigs at all time points following initiation of treatment, with the greatest difference observed at day 28 (42.4 +/- 4.9 pg/ml in controls vs. 65.4 +/- 4.7 pg/ml in pGH-treated pigs). Serum 24,25-dihydroxy-vitamin D tended to be lower in pGH-treated pigs than in control pigs, being significantly lower on day 21 of the experiment (3.22 +/- .52 vs. 6.73 +/- 1.22 ng/ml, respectively). Serum concentrations of 25-hydroxyvitamin D and calcium were unaffected by pGH treatment. Kidneys of control pigs contained significantly more unoccupied vitamin D receptors than did kidneys from pGH-treated pigs (73.3 +/- 4.3 vs. 58.3 +/- 4.1 fmoles/mg protein). Duodenal tissue unoccupied vitamin D receptor content was similar in both pGH-treated (245 +/- 17.9 fmoles/mg protein) and control (263 +/- 21.8 fmoles/mg protein) pigs. Duodenal occupied vitamin D receptor concentration was similar in both pGH-treated (6.8 +/- .75 fmoles/mg protein) and control pigs (5.32 +/- .77 fmoles/mg protein).(ABSTRACT TRUNCATED AT 250 WORDS)

Inadequate dietary copper is known to result in undesirable metabolic changes in rats and humans. Abnormal cardiac function, leading to sudden death, is a common finding when copper deficient rats are fed a 62% fructose diet. To further study the apparent mineral-carbohydrate relationship to cardiac physiology, 3 male and 3 female swine were randomly assigned to four groups (6 pigs per group) which were fed low copper (1.5 ppm) or copper supplemented (40 ppm) diets with 20% of calories from either fructose or glucose for 10 weeks. In agreement with results from other animal studies, copper deficient swine exhibited decreased plasma ceruloplasmin, erythrocyte superoxide dismutase and plasma lysyl oxidase activities and lowered serum copper. The copper deficient fructose group had the lowest aortic lysyl oxidase activity and hematocrit when compared to the other groups. The relative heart weight in the copper deficient fructose group was 93% greater than the other three dietary groups. The livers of copper deficient fructose fed pigs were also significantly larger. Two enzymes related to cardiac and hepatic function, aspartate and alanine aminotransferase were also measured. Copper deficiency significantly lowered alanine aminotransferase but there was no dietary effect on aspartate amino-transferase. The results of this project indicate that the pig is a sensitive model for the study of cardiovascular abnormalities which occur when fructose is consumed with a low copper diet.

Thirty-seven pigs with an initial live weight of 60 kg were used to investigate the effects of daily exogenous porcine somatotropin (pST) administration at two dose levels (0 and 100 micrograms.kg-1.d-1) for a 31-d period on muscle fiber characteristics and meat tenderness of boars, gilts and barrows. Excipient boars and gilts had more alpha W and fewer alpha R fibers than did those receiving pST. The percentage of muscle fiber type for barrows was not affected by pST treatment. The administration of pST resulted in an increase in muscle fiber size for all three fiber types in all three sexes, but these changes were of greater magnitude in barrows (31.8%) and gilts (27.8%) than in boars (9.3%). Somatotropin negated the intrinsic sex effect differences in fiber area of the pigs. There was no difference in tenderness among excipient boars, barrows and gilts; however, with the inclusion of pST, shear force decreased in boars and gilts and increased in barrows. A high proportion of the pST-treated pigs contained giant fibers in the longissimus muscle. Furthermore, a small proportion of the pST-treated pigs exhibited pale, soft, exudative muscle. Whether the giant fiber anomalies occurred through increased muscle activity or from fibers undergoing degenerative changes was not determined.

An experiment with crossbred swine was conducted over six generations of selection based on an index (Index) of average daily gain in weight (ADG) in a test period from 56 d of age to 91 kg gross weight and average backfat thickness (ABF) measured from ultrasonic scans at 91 kg. Test pigs of the high protein select (HS) and control (HC) lines were fed a 24% crude protein (CP) diet and pigs of the low protein select (LS) and control (LC) lines were fed a 12% CP diet during the test period. The extent of genetic (selection line) x environmental (dietary) interaction effects was determined based on feeding closely related boars and gilts from both the HS and LS lines on both diets. Tests were conducted in 1986 and 1987 with progeny of the fifth and sixth generations of selection. Records for 472 pigs sired by 37 boars and out of 101 dams were analyzed for effects of selection and diets on AGE of pig at 91 kg, ADG, ABF, LMA (longissimus muscle area at the last rib) and Index. Statistically significant interactions effects of line x diet were noted (P less than .01) for AGE, ADG and Index, traits with low to moderate heritabilities (h2). For ABF and LMA, body composition traits with moderate or higher h2, interaction effects of line x diet were near zero. These results suggest that for best all-around future performance, traits such as AGE and ADG, selection probably should be practiced under dietary conditions under which future populations will be produced. For body composition traits such as ABF and LMA, selection probably would be more effective if pigs were fed a more enriched protein diet. However, as a practical matter, to more rapidly improve the genetic merit of the swine population, both the central station and on-the-farm testing programs should be conducted under standard commercial production systems.

Two experiments were conducted with young, growing pigs to evaluate the effects of protein levels and supplemental lysine on growth, body characteristics and urea cycle enzyme activities. In the first experiment, 8-week-old pigs weighing 17 kg were fed two levels of protein (12 or 20%) until they reached slaughter weight of approximately 95 kg. In the second experiment, three levels of protein (12, 18 or 24%) and one level of additional lysine (9 g/kg of diet added to the 12% protein diet) were fed for the same interval. After slaughter, urea cycle enzyme activities (argininosuccinate synthetase, EC 6.3.4.5; argininosuccinate lyase, EC 4.3.2.1; and arginase, EC 3.5.3.1) were determined in liver homogenates. Early growth of pigs was improved by increasing the protein level (12%) but not by adding the limiting amino acid lysine to the 12% diet. The cross sectional area of the Longissimus dorsi muscle at slaughter was increased by protein level (12%) or by adding lysine to the 12% protein diet. In contrast, subcutaneous fat was decreased only by increasing the dietary protein level. The activities of arginase, argininosuccinate synthetase and argininosuccinate lyase were increased in a linear fashion by increasing the dietary protein level. In contrast, adding lysine to the 12% protein diet did not increase urea cycle enzyme activities.