Changes in the expression of uncoupling proteins and lipases in porcine adipose tissue and skeletal muscle during feed deprivation*(1).

The hormone-sensitive and lipoprotein lipases are critical determinants of the metabolic adaptation to starvation. Additionally, the uncoupling proteins have emerged with potential roles in the metabolic adaptations required by energy deficiency. The objective of this study was to evaluate the expression (mRNA abundance) of uncoupling proteins 2 and 3 and that of hormone-sensitive and lipoprotein lipase in the adipose tissue and skeletal muscle of the pig in relationship to feed deprivation. Thirty-two male castrates (87 kg +/- 5%) were assigned at random to fed and feed-deprived treatment groups. After 96 hr, the pigs were euthanized and adipose and skeletal muscle tissue obtained for total RNA extraction and nuclease protection assays. Feed deprivation increased uncoupling protein 3 mRNA abundance 103-237% (P < 0.01) in longissimus and red and white semitendinosus muscle. In contrast, the increase in uncoupling protein 3 mRNA in adipose tissue was only 23% (P < 0.06), and adipose uncoupling protein 2 mRNA was not influenced (P > 0.66) by feed deprivation. The increased abundance of uncoupling protein 2 mRNA in the longissimus muscle of feed-deprived pigs was small (22%), but significant (P < 0.04). The expression of hormone-sensitive lipase was increased 46% and 64% (P < 0.04) in adipose tissue and longissimus muscle, respectively, by feed deprivation, whereas adipose lipoprotein lipase expression was reduced (P < 0.01) to 20% of that of the fed group. Longissimus lipoprotein lipase expression in the feed-deprived group was 37% of that of the fed group (P < 0.01), and similar reductions were detected in red and white semitendinosus muscle. Overall, these findings indicate that uncoupling protein 3 expression in skeletal muscle is quite sensitive to starvation in the pig, whereas uncoupling protein 2 changes are minimal. Furthermore, we conclude that hormone-sensitive lipase is upregulated at the mRNA level with prolonged feed deprivation, whereas lipoprotein lipase is downregulated.

Regulation of PPARgamma but not obese gene expression by dietary fat supplementation.

Leptin, the product of the obese gene, and peroxisome proliferator activated receptor gamma (PPARgamma) are important regulators of energy metabolism, adipogenesis, and immune function. In rodent models, both genes seem to respond at the mRNA and/or protein levels to dietary fat consumption. To determine the effect(s) of dietary saturated and polyunsaturated fatty acids on the expression (mRNA abundance) of these genes, adipose tissue was obtained from pigs fed three different dietary fat sources. Corn-soybean meal diets containing no added fat (NO, control) or 10% beef tallow (BT), safflower oil (SO), or fish oil (FO) were fed ad libitum (n = 12) for 12 weeks. The abundance of obese, PPARgamma1, and PPARgamma2 mRNA was quantified relative to 18S rRNA using ribonuclease protection assays. The gain:feed ratio was improved (P < 0.05) 21% by all fats with a corresponding reduction (P < 0.05) in feed intake. Relative to pigs fed NO, serum total cholesterol was increased (P < 0.01) in pigs fed BT and triglyceride and nonesterified fatty acid concentrations were increased (P < 0.01) by all supplemental fats. Serum insulin was increased (P < 0.10) only by SO. Neither obese nor PPARgamma1 mRNA abundance were responsive to added fat (P > 0.15). However, the abundance of PPARgamma2 mRNA was increased fourfold by SO compared with the NO diet. These data indicate that the abundance of obese mRNA is independent of dietary fat consumption per se, whether saturated or unsaturated, when feed consumption is reduced due to greater dietary caloric density. Furthermore, we provide evidence that expression of the PPARgamma2 gene in porcine adipose tissue is selectively responsive to SO (presumably linoleic acid, 18:2n-6).

Soybean isoflavones, genistein and genistin, inhibit rat myoblast proliferation, fusion and myotube protein synthesis.

The isoflavones, genistein and genistin, are cytotoxic in vitro (e.g. , inhibition of cell proliferation), due in part to inhibition of protein tyrosine kinase and DNA topoisomerase activities. Normal cell functions associated with these enzymatic activities could potentially be impaired in animals through ingestion of soybean products. In this study, cultured rat myogenic cells (L8) were used to determine whether genistein or genistin influences myoblast proliferation and fusion, and myotube protein synthesis and degradation. Genistein or genistin was dissolved in dimethylsulfoxide and included in the culture medium at 0, 1, 10 or 100 micromol/L. Myoblast proliferation was measured by methyl-3H-thymidine incorporation over 48 h. Myoblast differentiation was evaluated by the number of nuclei in multinucleated myotubes. Myotube protein synthesis was measured by 2-h 3H-amino acid incorporation into the myosin and total protein pools after acute (2 h) or chronic (24 h) exposure to similar treatments; protein degradation was measured by measuring radioactivity in protein pools following a time course of protein breakdown after myotube proteins were prelabeled with 3H-amino acids. Genistein or genistin strongly inhibited in vitro myoblast proliferation (P < 0.001) and fusion (P < 0.001) in a dose-dependent manner with effective genistein concentration as low as 1 micromol/L. Genistein or genistin inhibited protein accretion in myotubes (P < 0.001). Decreased protein accretion is largely a result of inhibition on cellular (myofibrillar) protein synthesis rate. No adverse effect on protein degradation was observed. Results suggest that if sufficient circulating concentrations are reached in tissues of animals consuming soy products, genistein/genistin can potentially affect normal muscle growth and development.

Myostatin expression in porcine tissues: tissue specificity and developmental and postnatal regulation.

The objective of this study was to establish the developmental pattern and tissue specificity of porcine myostatin expression and to evaluate expression in skeletal muscle during circumstances in which muscle growth was altered. Northern blot analysis revealed two transcripts (1.5 and 0.8 kb). Myostatin mRNA was detected in whole fetuses at 21 and 35 days and was markedly increased (P < 0.05) by 49 days. At birth, mRNA abundance in longissimus muscle had declined significantly (P < 0.05) from that at day 105 of gestation and continued to decrease (P < 0.05) to its lowest level 2 wk postnatally (4 kg body wt). Myostatin expression was higher (P < 0. 05) at 55, 107, and 162 kg body wt than at 4 kg body wt. Postnatally, myostatin mRNA was detected in skeletal muscle and mammary gland. Expression at birth was 65% higher (P < 0.04) in longissimus muscle of low-birth-weight piglets (0.57 +/- 0.052 kg body wt) vs. normal (1.37 +/- 0.077 kg body wt) littermates, irrespective of gender. However, suppression of longissimus muscle growth by food deprivation (3 days) did not alter (P > 0.15) myostatin expression in either 4- or 7-wk-old piglets. Additionally, myostatin mRNA abundance was not changed by porcine growth hormone administration in growing animals. These data indicate that myostatin expression in skeletal muscle peaks prenatally and that greater expression is associated with low birth weight. Expression in mammary gland indicates a possible role for myostatin in mammary gland development and/or lactation.

Porcine somatotropin improves growth in finishing pigs without altering calpain 3 (p94) or alpha-actin mRNA abundance and has a differential effect on calpastatin transcription products.

The objective of this study was to determine whether the improvements in growth and efficiency of gain achieved by recombinant porcine somatotropin (pST) are associated with altered expression of the p94, calpastatin, or alpha-actin genes in porcine longissimus (LD) muscle. Forty-eight barrows (initial 64.2 to 67.4 kg BW) were assigned to four treatments (n = 12) arranged as a 2 x 2 factorial in a randomized complete block design. Factors were duration of treatment (3 or 6 wk) and pST administration (0 or 3 mg x pig(-1) x d(-1)). Plasma samples were obtained 24 h after the first pST injection and at the end of the each treatment period for assays of selected variables. The LD samples were obtained at 3 and 6 wk of pST treatment. Northern blot analysis of calpastatin expression in LD muscle revealed three distinct transcription products of approximately 8.5 (CPST I), 5.5 (CPST II), and 2.5 (CPST III) kb; CPST II was reduced (P < .02) 33 and 61% by pST at 3 and 6 wk, respectively, whereas CPST I and III were not influenced (P > .12). Neither alpha-actin nor p94 was responsive to pST injection. As expected, pST resulted in higher (50%, P < .02) plasma insulin within 24 h and one- and twofold higher (P < .01) concentrations at 3 and 6 wk, respectively. Glucose was increased (P < .01) at 3 (15%) and 6 (10%) wk, whereas urea nitrogen was reduced (32 to 36%, P < .01). The efficacy of pST was evident in that ADG was improved (P < .01) 11 to 13% independent of time. Likewise, feed intake was reduced (P < .01) 10 to 11% and gain: feed improved (P < .01) approximately 26% for pigs receiving pST independent of time. These data indicate that the enhanced muscle growth achieved by pST is not associated with altered expression of p94 or alpha-actin, or an increase in the abundance of any calpastatin transcription product.

Obese gene expression in porcine adipose tissue is reduced by food deprivation but not by maintenance or submaintenance intake.

The relationship between obese gene expression and energy intake was determined in pigs of various body weights. With ad libitum consumption, expression increased (P < 0.001) with body weight from 55 to 163 kg. Obese mRNA relative abundance was correlated with fat mass (r = 0.74, P < 0.0001) and percentage of fat (r = 0.72, P < 0. 0001). Obese expression was also evaluated at 159 kg (initial weight) and ad libitum, maintenance or 23% of maintenance intake for 28 d. Obese mRNA was independent of treatment (P > 0.78) despite considerable weight differences. Obese mRNA abundance was then compared at 136 kg (initial weight) and ad libitum or maintenance intake for 3 or 28 d. Abundance was not influenced by either duration of treatment or intake, despite a small increase (P < 0.01) in serum nonesterified fatty acids (NEFA) and a reduction (P < 0.02) in insulin attributable to maintenance intake. Finally, mRNA abundance was determined at 60 and 136 kg and conditions of food deprivation or ad libitum intake for 3 d. Food deprivation reduced (P < 0.01) serum insulin and increased (4- to 5-fold) NEFA concentrations. Obese mRNA abundance was greater (P < 0.01) in the heavier pigs and was reduced (P < 0.01) by food deprivation. We conclude that obese mRNA abundance in pigs correlates with fat mass and percentage of body fat under conditions of ad libitum intake. Furthermore, obese mRNA abundance is reduced by food deprivation, whereas lesser degrees of intake restriction do not change obese mRNA abundance, even when accompanied by appreciable weight loss.

Leptin expression in porcine adipose tissue is not increased by endotoxin but is reduced by growth hormone.

The physiologic response to infection includes reductions in tissue concentrations of anabolic growth factors as a means of reducing growth and conserving nutrients for immunologic processes. This repartitioning of nutrients is accompanied by anorexia, which has been linked to increased leptin expression. Furthermore, leptin and growth hormone (GH) concentrations are inversely related, with leptin being required for normal GH release. The objective of this study was to determine if pretreatment with GH would influence endotoxin-induced changes in leptin expression or attenuate endotoxin-induced reductions in serum insulin-like growth factor-1 (IGF-1) and IGF-1 expression in liver and longissimus muscle. In experiment 1, 40 pigs were assigned to four treatments (n = 10 per treatment) arranged as a 2x2 factorial with GH (s.c. injection, 2 mg 1 h before challenge and 2 mg 2 h after challenge) and endotoxin (single i.m. injection, 25 microg/kg body weight) as main effect variables. Pretreatment with GH resulted in a marked increase (p<0.001) in serum GH within 1 h that was sustained throughout the study. Endotoxin challenge reduced (p<0.003) serum IGF-1 independent of GH (GH x endotoxin, p>0.682), and reduced (p<0.05) IGF-1 expression in longissimus muscle but not liver. Leptin mRNA abundance was reduced 56% (p<0.005) by GH but was not affected by endotoxin (p>0.81). In experiment 2, 36 pigs (n = 12 per treatment) were either allowed ad libitum feed consumption with no injection or deprived of feed and injected twice with either saline or endotoxin 24 h apart. Feed deprivation reduced leptin expression (p<0.05). However, endotoxin did not change leptin expression but markedly increased (p<0.05) serum haptoglobin. These data indicate that changes in IGF-1 status in endotoxin-challenged pigs are independent of serum GH and that leptin expression is not increased by endotoxin challenge in the pig. These data also indicate a regulatory linkage between GH and leptin in vivo.

Effect of dietary energy source and immunological challenge on growth performance and immunological variables in growing pigs.

Forty-eight growing pigs (23 kg BW) were assigned to four treatments (n = 12) arranged as a 2 x 2 factorial. Dietary energy source (conventional [CON] vs high-oil corn [HOC]), with or without an immunological challenge (IC) regimen constituted main effects. The IC regimen consisted of injection of endotoxin (E. coli lipopolysaccharide [LPS]) and vaccination for porcine respiratory and reproductive syndrome (PRRS). Growth performance data were collected over a 5-wk period and are presented as prechallenge (d 1 to 14; d 1 was the 1st d of the study), challenge (d 15 to 21), and postchallenge (d 22 to 36) periods, and overall. Overall, the pigs fed HOC consumed less feed (P < .11) and gained more efficiently (P < .03). During the immunological challenge period, ADG was depressed 21% and feed intake 15% (P < .01). The IC resulted in lower (P < .01) serum alpha-1-acid glycoprotein (AGP) concentrations on d 22, and the magnitude of the reduction was greater in the pigs fed the CON diet (energy source x immune challenge, P < .10). Serum AGP concentrations remained lower (P < .08) in challenged pigs on d 36. Immunoreactive prostaglandin concentrations were higher (55%, P < .08) in the pigs fed HOC immediately following the IC period (d 22). The data reported herein indicate that the performance of pigs fed HOC is satisfactory, and that feeding HOC does not compromise growth performance during or after an immunological challenge.

Influence of gilt age and body composition at first breeding on sow reproductive performance and longevity.

Regression analysis was used to evaluate the effects of gilt age and body composition at first breeding on sow performance over three parities. Eighty-seven Yorkshire x Landrace F1 gilts were used. Variation in age and body composition at first breeding was obtained by breeding gilts at puberty, second, or third estrus and by providing those gilts bred after puberty one of four nutritional regimens from puberty until breeding: 1) 2.7 kg/d of a 14.3% CP, 3.5 Mcal ME/kg diet (H), 2) maintenance ME and CP/d (M), 3) half-maintenance ME and CP/d (1/2M), and 4) M or 1/2M until anestrus, then 2.27 kg/d of a 14.0% CP corn-soybean meal diet until first breeding. Body composition at first breeding was determined using live weight, backfat thickness, and deuterium oxide space as variables in prediction equations. All females were treated similarly after first breeding. Age and body composition at first breeding were not related (P > .10) to litter size at birth or weaning in parities 1, 2, 3, or overall. Increasing age at first breeding was related to small increases in pig birth weights (P < .001) in parity 1 and average pig weaning weight (P < .001) in parities 1, 2, and overall. Body composition of gilts at first breeding was not related (P > .10) to pig birth weights and was inconsistently related to pig weaning weights in parities 2 and 3 (P < .001). Females heavier at first breeding remained heavier (P < .01) throughout the experiment. Age and body composition at first breeding were not different (P > .10) for gilts completing three parities (n = 53) compared with gilts failing to complete three parities (n = 34). Results show no large effects of gilt age or body composition at first breeding on sow productivity and longevity over three parities.

Effect of adding fat and(or) milk products to the weanling pig diet on performance in the nursery and subsequent grow-finish stages.

Six experiments were conducted to evaluate the use of fat in diets containing a high level of milk products for weanling pigs. In Exp. 1, 192 pigs (6.6 kg and 23 d) were used to determine whether milk products (0 or 40%) in the diet influenced the utilization of fat (0 or 10%). No fat x milk product interactions were found. Adding milk products to the diet improved (P < .01) ADG, ADFI, and gain/feed (G/F). Adding fat to the diet did not influence performance. In Exp. 2, 3, and 4, 576 pigs (6.0 kg and 20 d) were used to determine the influence of fat level on performance. Adding soybean oil (0, 3, 6, or 9%) to the diet from d 0 to 14 after weaning had no influence on growth performance. Increasing soybean oil (0, 2, 4, or 6%) in the diet from d 14 to 35 had no influence on ADG; however, G/F improved linearly (P < .001). In Exp. 5, 196 pigs (7.5 kg and 26 d) were used to determine the influence of fat source (soybean oil, corn oil, or tallow) on performance. Pig performance was not different among fat sources. In Exp. 6, 240 pigs (5.4 kg and 21 d) were used to determine the influence of fat and(or) milk product inclusion in the nursery diet on subsequent grow-finish performance. Adding milk products, but not fat, to the nursery diet improved (P < .08) overall performance to market weight. These results indicate adding fat to the diet from d 0 to 14 after weaning had no influence on performance. Adding fat to the diet from d 14 to 35 improved G/F; however, it did not improve ADG or overall performance to market. Diet composition during the nursery period can affect subsequent performance.

Body composition of gilts at puberty.

The relationship between body composition and the occurrence of puberty was evaluated using 93 Yorkshire x Landrace gilts. At approximately 60 d of age gilts were purchased and placed in a heated confinement unit where they were housed for the duration of the study. Ad libitum access to feed was provided throughout the study. Gilts were moved, mixed, and initially exposed to mature boars at approximately 120 d of age to encourage the earliest possible occurrence of puberty. Empty body weights of water, fat, protein, and ash at puberty were estimated using a deuterium dilution technique and prediction equations developed for this gilt population. There was considerable variation in age, weight, and all measures of body composition at puberty. Gilts were 138 to 240 d old and weighted 64.9 to 150.8 kg. Backfat thickness ranged from 17.5 to 44.0 mm. Gilts were composed of 32.4 to 64.3 kg of water, 15.6 to 53.9 kg of fat, 9.03 to 20.56 kg of protein, and 1.24 to 3.10 kg of ash. The coefficient of variation for fat to lean ratio at puberty was 15.39%. Linear and quadratic regressions showed that lifetime (birth to puberty) growth rate was not related to age at puberty (P > .10). Based on the variation in body composition observed it was concluded that the occurrence of puberty in gilts given ad libitum access to feed during rearing and initially exposed to mature boars at approximately 120 d of age was not related to certain minimum threshold amounts of body tissues or to a specific rate at which body tissue reserves were accumulated.

In vivo estimation of body composition of mature gilts using live weight, backfat thickness, and deuterium oxide.

Thirty-seven Duroc x (Yorkshire x Landrace) (DYL) and 21 Yorkshire x Landrace (YL) gilts were used to develop equations that predict body composition of replacement-age breeding swine. Before slaughter, gilts were weighed, ultrasonically scanned for 10th rib backfat thickness, and infused with D2O (.25 g/kg live weight). The D2O space (kilograms) was calculated from body water D2O concentration determined at equilibrium (150 and 210 min after infusion). Regression models predicting empty body (Eb) components for DYL and YL groups were fitted using all possible variable combinations (D2O space, live weight, and[or] backfat depth). Variables selected in best-fit models for Eb water, protein, fat, and ash for data from DYL gilts differed from variables selected from data from YL gilts. Average prediction errors (kilograms; [predicted residual sum of squares divided by n]1/2) of best-fit equations were 2.37, 2.03 (Eb weight), 2.36, 1.66 (Eb water), 1.07, .47 (Eb protein), and 2.76, 2.89 (Eb fat) for DYL and YL data sets, respectively. Cross-validation by applying DYL equations to YL data, and vice versa, resulted in larger prediction errors. Likewise, larger errors were obtained when equations published elsewhere were applied to DYL and YL data sets. No cited source provided a set of equations that consistently minimized prediction errors of all Eb components of both DYL and YL gilts. Results indicate that prediction equations using D2O space, live weight, and(or) backfat thickness are accurate in estimating body composition only in animals physiologically resemble the population in which the equations were derived.

Lecithin in swine diets: I. Weanling pigs.

One digestibility experiment (Exp. 1) and two growth experiments (Exp. 2 and 3) were conducted to evaluate the use of lecithin as an emulsifier of soy oil and(or) an energy source in a two-phase starter diet program. Phase 1 consisted of d 0 to 14 postweaning, and Phase 2 consisted of d 14 to 35 postweaning. Diets were based on corn, soybean meal, and 20% dried whey and contained a constant ME:lysine level. In Exp. 1 and 2, two levels of lecithin (0 and 2%) at two levels of soy oil (0 and 6%) were investigated. In both experiments, there was no interaction between lecithin and soy oil for any traits measured. In Exp. 1, the apparent digestibility of fat increased significantly with increased fat level in the diets. Addition of lecithin to diets improved (P < .05) nitrogen retention, and the addition of soy oil significantly improved apparent digestibility of DM, GE, fat, and CP. In Exp. 2, there was no significant effect of lecithin or soy oil on ADG. In Phase 2 and overall, the inclusion of lecithin and soy oil to diets significantly increased gain/feed but did not significantly improve gain/ME intake. In Exp. 3, pigs were fed diets containing 0, 1, 2, or 3% lecithin. The addition of lecithin to diets did not affect ADG, ADFI, gain/feed, or gain/ME intake during Phases 1, 2, or overall. These results fail to demonstrate that the addition of lecithin to diets for young pigs improves utilization of soy oil or growth performance.

Lecithin in swine diets: II. Growing-finishing pigs.

Lecithin was investigated in diets for growing-finishing pigs. Diets were based on corn and soybean meal and contained a constant ME:lysine level. The use of lecithin as an emulsifier on utilization of soy oil by the pig was investigated in Exp. 1. Diets were arranged in a 2 x 2 factorial structure with two levels of lecithin (0 and 2%) and two levels of soy oil (0 and 6%). There were no interactions between lecithin and soy oil for any measurements of growth performance. In general, the inclusion of lecithin or soy oil did not affect (P > .1) ADG but did improve (P < .01) gain/feed during the finishing period and during the entire experiment. During the finishing period, gain/ME intake was improved (P < .01) by both lecithin and soy oil. The use of lecithin as an energy source for pigs was investigated in Exp. 2. Dietary treatments were corn and soybean meal diets with 0, 1, 2, or 3% lecithin. There were no significant differences in performance of pigs as measured by ADG, ADFI, gain/feed, and gain/ME intake among the four lecithin levels. Lecithin did not improve utilization of soy oil by growing-finishing pigs. Furthermore, lecithin was not an efficacious source of supplemental dietary fat for growing-finishing pigs in this study.

Body composition of postpubertal gilts at nutritionally induced anestrus.

An experiment using comparative slaughter was conducted to examine the relationship between occurrence of nutritionally induced anestrus in postpubertal gilts and chemically determined body composition and body composition changes. Thirty-nine Duroc x (Yorkshire x Landrace) gilts, each having experienced three or more estrous cycles, were used. Nine gilts were chosen randomly, weighed, ultrasonically scanned for 10th rib backfat thickness, and slaughtered to determine initial body composition. Remaining gilts were allotted randomly to five dietary treatments, four characterized as severely energy restrictive (RES; .25, .50, .75, and 1.0 mcal of ME/d) and a control (3.4 Mcal of ME/d). Dietary treatments provided equal amounts of protein (50 g), minerals, and vitamins daily. Individual serum progesterone levels were determined every 3 d using RIA and gilts were considered anestrous when concentrations were < 1.0 ng/mL for four consecutive samples (9 d). All RES gilts became anestrous, and gilts restricted more severely tended (P = .22) to do so more quickly. Days to anestrus were 66.0 +/- 12.0, 77.4 +/- 13.1, 84.5 +/- 12.0, and 86.5 +/- 12.0 for treatments .25, .50, .75, and 1.0, respectively. Among RES treatments there were no linear, quadratic, or cubic effects of ME intake (P > .10) on the quantity of body protein or fat lost, or on the quantity of body protein or fat remaining at anestrus. However, individual body protein and body fat contents of RES gilts at slaughter revealed that anestrus occurred at a wide range of body compositions, from 13.4 to 20.2 kg of protein and .36 to 27.0 kg of fat. This wide range of individual values suggests that estrous activity in the mature gilt is not controlled by specific threshold levels of body reserves.

Estrous cycle characteristics of postpubertal gilts approaching anestrus due to limited dietary energy intake.

Twenty-nine Duroc x (Yorkshire x Landrace) gilts, approximately 9 mo of age and each having experienced at least three estrous cycles, were allotted randomly to five dietary treatments. Each treatment provided a different daily intake of metabolizable energy: .25, .5, .75, 1.0 Mcal (severely restrictive [RES]; chosen to cause cessation of estrous cycles) or 3.4 Mcal (control; designed for maintenance of estrous cyclicity). Blood samples were drawn by venipuncture every 3 d and sera were assayed for progesterone (P4) concentration. Estrous cycle length was estimated by defining d 0 as the last day when serum P4 concentrations were < 1 ng/mL before increasing to > 1 ng/mL. Gilts were considered acyclic when serum P4 levels remained < 1 ng/mL for four consecutive samples (9 d). Anestrus occurred after 78.7 +/- 6.1 d in all RES gilts (n = 23) and in one control on d 24. Compared with the control treatment, RES treatments resulted in longer (P < .05) average estrous cycles (21.0 +/- .2 vs 20.2 +/- .3 d) and greater (P < .05) mean serum P4 concentrations (13.7 +/- .4 vs 11.4 +/- .8 ng/mL). There were no differences in P4 or cycle length measurements among RES treatments. Cycle duration and serum P4 concentrations of the final estrous cycle before anestrus were similar to those of previous cycles. It is concluded that severe energy restriction caused elevated serum P4 concentrations. Neither cycle length nor serum P4 concentration was notably altered as gilts neared anestrus.

Antimicrobial supplementation of growing pigs: the effect of porcine sera fractions on in vitro muscle cell proliferation.

Sera obtained from pigs before and after subtherapeutic levels of ASP250 supplementation (pre and post serum pools) have been subjected to comparative fractionation by using gel filtration and affinity chromatography on immobilized Cibacron Blue F3G-A. Comparable serum fractions obtained from pre- and post-ASP250 blood sera were assayed in muscle cell culture bioassays designed to measure their effect on proliferation. Pre- and post-ASP250 sera were subjected to gel filtration and divided into the following fractions: fraction 1, Kav less than .17; fraction 2, Kav = .17 to .41; fraction 3, Kav = .41 to .59. Post-ASP250 fractions 2 and 3 increased proliferation rate in cultured muscle cells to a greater extent than comparable pre-ASP250 fractions (P less than .001). Chromatography of fraction 3 on immobilized Cibacron Blue F3G-A showed that both pre- and post-ASP250 fraction 3 contained a putative inhibitor of myogenic cell proliferation as well as mitogenic factors. However, negative growth factor activity was greater in pre-ASP250 fraction 3 than in post-ASP250 fraction 3 (P less than .05). Additionally, positive growth factor activity was lower in pre-ASP250 fraction 3 than in post-ASP250 fraction 3 (P less than .05). These data suggest that levels and(or) activities of both positive and negative muscle growth factors in serum may be altered by the addition of antimicrobials to the diets of growing pigs.

In vitro muscle cell proliferation and protein turnover as affected by serum from pigs fed antimicrobials.

The effect of antimicrobial supplementation of pigs on the capacity of their sera to influence proliferation and protein turnover in cultured muscle cells was evaluated. Mitogenic activity of sera increased when pigs were fed ASP250 (P less than .005) or carbadox (P less than .001), whereas the mitogenic activity of serum from pigs receiving the basal diet remained unchanged (P = .5). Additionally, sera from ASP250-fed pigs significantly decreased (P less than .001) total cellular protein degradation compared with sera obtained from the same pigs prior to supplementation. Neither ASP250 nor carbadox stimulated proliferation of myogenic cells when added to the culture media. Inclusion of ASP250 in swine diets altered the composition of their sera in a way that stimulated muscle cell proliferation and reduced the rate of protein degradation in cultured myogenic cells. Likewise, the inclusion of carbadox in swine diets increased the ability of their sera to stimulate cultured muscle cell proliferation.

Limits of medium-chain and long-chain triacylglycerol utilization by neonatal piglets.

Fifteen unsuckled neonatal piglets from three litters were fasted for 2 h after birth then allotted within litter to a 2 x 3 factorial arrangement of treatments and given by stomach tube 2.36, 4.91 or 11.32 g of either (1-14C)-triolein or (1-14C)-trioctanoin/BW (kg).75. The hourly 14CO2 production was measured for 12 h for estimating the oxidation rate of dosed triacylglycerols. The contents of each segment of the digestive tract were collected for 14C and lipid analyses for calculating absorption of the dosed triacylglycerols. Grams of trioctanoin absorbed (P less than .01) and oxidized (P less than .001) by piglets were higher than grams of triolein. The maximum amounts of trioctanoin and triolein absorbed in 12 h were 2.77 +/- .29 and 1.83 +/- .36 g/BW (kg).75, respectively. The maximum amounts of trioctanoin and triolein oxidized in 12 h were 1.60 +/- .14 and .33 +/- .17 g/BW (kg).75, respectively. The maximum amounts of trioctanoin and triolein oxidization during 1-h periods were .231 +/- .017 and .049 +/- .021 g/BW (kg).75, respectively. The calculated maximum percentage of piglets' daily maintenance energy needs supplied by trioctanoin oxidation was 42.0%, compared with 10.6% from triolein. The maximum utilization of trioctanoin occurred at the intermediate dose. Results indicated that trioctanoin was used more effectively than triolein; it may be useful as a source of supplemental energy to improve the survival of piglets. A single dose should provide about 6 g/body wt (kg).75.

Digestion and absorption of fish oil by neonatal piglets.

In order to establish the digestibility and absorption of fish oil, 18 unsuckled, newborn piglets were tube-fed an amount of fish oil calculated to provide the piglets' maintenance energy needs for 12 h. After fat administration the piglets were either intubated with 25 ml of fat-free milk replacer per h, or fasted. The digesta of the stomach, small intestine, and large intestine (digesta plus feces) were collected 12 h after fish oil intubation. Disappearance of total extractable fat was 95 +/- 1 and 94 +/- 1% for fed and fasted piglets, respectively. True absorption of the lipid was calculated from the disappearance of eicosapentaenoic acid and was 99% for both fed and fasted piglets. Nearly 50% of the stomach lipid was as diglycerides and free fatty acids, suggesting that hydrolysis of the fish oil was initiated in the stomach. Small intestinal lipid was 63-65% free fatty acids, indicating that the piglet pancreatic lipase was of sufficient activity to hydrolyze fish oil triglyceride. Neonatal piglets appeared to have ample capacity to digest and absorb fish oil, which supports the concept that lipid supplementation could improve the energy status of the newborn piglet.