Insulin binding to mouse adipocytes exposed to clenbuterol and ractopamine in vitro and in vivo

Insulin binding to mouse adipocytes was measured after in vitro (30 min) and in vivo (5 days) exposure to clenbuterol and ractopamine. At 10(-6) M, both agonists decreased insulin binding by 20-30% after a 30 min preincubation at each insulin concentration between 1 and 25 ng/ml. Binding was not decreased if propranolol was present. Scatchard plots suggested that decreased binding was due to a decrease in insulin receptor concentration. Insulin binding was decreased approximately 10% at agonist concentrations as low as 10(-13) M, but binding was not further decreased until concentrations exceeded 10(-9) M. Rate of gain was increased 2-fold by clenbuterol (10 mg/liter of drinking water) and 50% by 500 mg ractopamine/liter, but not by 50 mg ractopamine/liter. Clenbuterol and ractopamine (500 mg/liter) decreased fat pad weight but only clenbuterol increased hind limb muscle mass. Insulin binding following in vivo administration was not influenced by ractopamine at 50 mg/liter, but tended to be increased by clenbuterol and ractopamine at 500 mg/liter. The disparity in results between administering the beta-agonists in vitro or in vivo suggests that counter regulatory factors influenced insulin binding capacity in vivo. Results indicate that ractopamine and clenbuterol can decrease insulin binding to adipocytes but the relevance of this response to decreased fat accretion is not clear.     

Characterization of porcine beta1- and beta2-adrenergic receptors in heart, skeletal muscle, and adipose tissue, and the identification of an atypical beta-adrenergic binding site

The objective of this study was to characterize porcine beta1- and beta2-adrenergic receptors (beta1-AR and beta2-AR) in heart, skeletal muscle, and adipose tissue by measuring the binding of a radioligand to cell membrane fragments. In skeletal muscle (LM), [3H]CGP12177 labeled a homogeneous population of beta2-AR as evidenced by the rank order of affinity of catecholamines [(-)isoproterenol > (-)epinephrine > (-)norepinephrine], a high affinity of the binding site for the beta2-AR-agonist clenbuterol (equilibrium dissociation constant, Kd = 16 nM), and a low affinity of the binding site for the beta1-AR-antagonist CGP20712A (Kd = 21 microM). The affinity of ICI118551, a ligand selective for beta2-AR in other species, was uncharacteristically low in porcine LM (Kd = 441 nM), but was consistent with a value reported for the cloned porcine beta2-AR. In heart ventricle, ligand binding revealed a predominant population of beta1-AR, judged by the rank order of affinity of catecholamines [(-)isoproterenol > (-)epinephrine > or = (-)norepinephrine] and high-affinity binding to CGP20712A (Kd = 40 nM). The Kd for ICI118551 (731 nM) was close to that observed at beta2-AR in LM, confirming that ICI118551 is not subtype-selective in the pig. Displacement studies using (-)propranolol, clenbuterol, and (-)isoproterenol revealed a second high-affinity binding site in the heart that was not a beta2-AR and could not be eliminated by guanosine 5'-triphosphate or guanylyli-midodiphosphate. In adipose tissue, an equal number of beta1- and beta2-AR was identified through the binding of clenbuterol and CGP20712A, whereas ICI118551 could not discriminate between these sites. In further experiments, we used 10 microM CGP20712A to eliminate beta1-AR binding and allow accurate Kd values to be determined at beta2-AR for nonselective ligands. Under these conditions, another binding site was observed that had a high affinity for (-)propranolol (Kd = 20 pM), which is inconsistent with beta3- or beta4-AR binding reported elsewhere. Our results indicate that porcine adipose tissue contains beta1-AR, beta2-AR, and an atypical binding site in the proportions 50, 34, and 16%, respectively, of the total binding sites labeled by [3H]CGP12177.     

Evaluation of the effects of dietary fat, conjugated linoleic acid, and ractopamine on growth performance, pork quality, and fatty acid profiles in genetically lean gilts

An 8-wk study of the effects of CLA, rendered animal fats, and ractopamine, and their interactive effects on growth, fatty acid composition, and carcass quality of genetically lean pigs was conducted. Gilts (n = 228; initial BW of 59.1 kg) were assigned to a 2 x 2 x 3 factorial arrangement consisting of CLA, ractopamine, and fat treatments. The CLA treatment consisted of 1% CLA oil (CLA-60) or 1% soybean oil. Ractopamine levels were either 0 or 10 ppm. Fat treatments consisted of 0% added fat, 5% choice white grease (CWG), or 5% beef tallow (BT). The CLA and fat treatments were initiated at 59.1 kg of BW, 4 wk before the ractopamine treatments. The ractopamine treatments were imposed when the gilts reached a BW of 85.7 kg and lasted for the duration of the final 4 wk until carcass data were collected. Lipids from the belly, outer and inner layers of backfat, and LM were extracted and analyzed for fatty acid composition from 6 pigs per treatment at wk 4 and 8. Feeding CLA increased (P < 0.02) G:F during the final 4 wk. Pigs fed added fat as either CWG or BT exhibited decreased (P < 0.05) ADFI and increased (P < 0.01) G:F. Adding ractopamine to the diet increased (P < 0.01) ADG, G:F, and final BW. The predicted carcass lean percentage was increased (P < 0.05) in pigs fed CLA or ractopamine. Feeding either 5% fat or ractopamine increased (P < 0.05) carcass weight. Adding fat to the diets increased (P < 0.05) the 10th rib backfat depth but did not affect predicted percent lean. Bellies of gilts fed CLA were subjectively and objectively firmer (P < 0.01). Dietary CLA increased (P < 0.01) the concentration of saturated fatty acids and decreased (P < 0.01) the concentration of unsaturated fatty acids of the belly fat, both layers of backfat, and LM. Ractopamine decreased (P < 0.01) the i.m. fat content of the LM but had relatively little effect on the fatty acid profiles of the tissues compared with CLA. These results indicate that CLA, added fat, and ractopamine work mainly in an additive fashion to enhance pig growth and carcass quality. Furthermore, these results indicate that CLA results in more saturated fat throughout the carcass.     

Adrenergic regulation of vascular smooth muscle tone in calf digital artery

Radioligand binding studies and functional assays on isolated smooth muscle preparations were performed in order to obtain a biochemical and functional characterization of the beta-adrenoceptor (beta-AR) subtypes involved in regulation of the smooth muscle relaxation of the calf's common digital artery. The results indicate that the common digital artery possesses two beta-AR populations (40% beta(1) and 60% beta(2)) and the beta(2)-subtype appears to predominate as far as function is concerned. Only the beta(2)-AR agonists clenbuterol and fenoterol caused dose-related relaxant effects, antagonized by propranolol, when tested in preparations precontracted both with PGF(2alpha) (1.4 x 10(-5) m) and noradrenaline (1.2 x 10(-6) m). In noradrenaline precontracted preparations the beta(1)-AR selective agonists dobutamine and xamoterol caused vasodilation which was not antagonized by (+/-)propranolol. While the functional relaxant effects of dobutamine may be attributed to its potent competitive alpha-AR blocking activity, further investigations are required to explain the effect of xamoterol. The vasodilator effect of (+/-)isoproterenol was irregular. The recorded contractile effects, mainly at dosages greater than 10(-6) m, suggest the loss of drug selectivity for beta-AR and alpha-AR activation. Indirect evidence indicates that the alpha-adrenoceptor (alpha-AR) population in this tissue which produces a strong contraction is functionally dominant over the beta-AR, suggesting limited therapeutic benefit for beta-AR drugs to control blood flow disorders in the calf's distal limb.     

Development of a model to describe the compositional growth and dietary lysine requirements of pigs fed ractopamine

The objective of this research was to use recent ractopamine research data to develop an updated mathematical model to describe the daily compositional growth of pigs fed ractopamine. Mean increases of 18.2, 23.1, and 25.0% for daily protein accretion were assumed for 5, 10, and 20 ppm of ractopamine for an overall gain of 40 kg of BW gain during the feeding period. The relative effect of ractopamine described the rapid increase and subsequent decrease in the effect of ractopamine as a function of BW gain or days on test and ractopamine concentration (RC, ppm). The reduction in ME intake produced by ractopamine was described as 0.036 x (RC/20)(0.7) multiplied by the ME intake for the first 20 kg of BW gain, and then increasing to 0.078 x (RC/20)(0.7) at 40 kg of BW gain feeding period. The ratio of fat-free muscle gain to protein accretion increased by 14 to 16% with the feeding of ractopamine, depending on the dietary lysine/essential AA levels. The ratio of carcass fat gain to empty body lipid gain was increased when lysine and essential AA requirements were met. Daily protein accretion and fat-free lean growth were described as functions of dietary lysine/essential AA intakes. The percentage of lysine in protein accretion increased with the feeding of ractopamine from 6.80 to 7.15%, depending on ractopamine concentration. Equations predicting carcass measurements, such as fat and longissimus muscle depths from carcass weight and composition, were modified to incorporate prediction biases produced by ractopamine. For the four concentrations of ractopamine (0, 5, 10, and 20 ppm, respectively) during a 78 to 110 kg of BW feeding period, the model predicted performance levels for ADG (1.03, 1.15, 1.16, and 1.16 kg/d), gain:feed (kg of ADG/kg of ADFI; 0.360, 0.401, 0.412, and 0.425), dressing percentage (75.1, 76.0, 76.3, and 76.4), percentage fat-free lean (48.7, 51.0, 51.5, and 52.2), longissimus muscle area (38.8,41.8,42.5, and 43.5 cm2), 10th-rib fat depth (22.1, 19.8, 19.3, and 18.7 mm), and fat-free lean gain (321, 446, 467, and 495 g/d), comparable to recent research data. The model allows the effect of ractopamine to be added to farm specific pig growth curves. It can be used to evaluate ways to optimize the use of ractopamine, including duration of ractopamine feeding, concentration of ractopamine, and dietary lysine concentration.     

Effect of beta-adrenergic agonists on lipolysis and lipogenesis by porcine adipose tissue in vitro

The effects of the beta-adrenergic agonists isoproterenol, cimaterol, ractopamine and clenbuterol on lipolysis (release of glycerol and free fatty acids) and lipogenesis (incorporation of 14C into fatty acids from [14C]glucose) was examined in porcine adipose tissue explants in vitro. Lipolysis was stimulated by isoproterenol, cimaterol or ractopamine but not by clenbuterol. Insulin reduced the lipolytic effects of the beta-adrenergic agonists (isoproterenol, cimaterol and ractopamine). Lipogenesis was inhibited by all beta-adrenergic agonists tested (isoproterenol, cimaterol, ractopamine and clenbuterol). The antilipogenic effect of the beta-adrenergic agonists was reduced by the presence of insulin in the incubation. Although effects of the different beta-adrenergic agonists varied, all had some direct effects that could be expected to reduce adipose accretion. Effects of beta-adrenergic agonists in the pig are due in part to direct effects on adipose tissue.     

Effect of fat type and forage level on performance of finishing cattle.

Four trials were conducted to determine the effects of adding various levels and types of fat to dry-rolled corn (DRC) finishing diets containing 0 or 7.5% forage. In Trial 1, 88 yearling steers (mean BW = 352 +/- 38 kg) and 176 heifers (mean BW 316 +/- 15 kg) were blocked by sex and weight into four replications. Treatments were 0, 2, 4, or 6% (DM basis) bleachable fancy tallow (BT) fed with 0 or 7.5% (DM basis) forage. Addition of BT to the 7.5% forage diet had no effect on ADG or gain/feed (G/F). However, adding BT to the all-concentrate diet decreased ADG (linear, P < .01) and G/F (linear, P = .08). In Trial 2, 184 yearling steers (mean BW = 347 +/- 21 kg) and 144 heifers (mean BW 322 +/- 8 kg) were blocked by sex and weight into six replications. Fat treatments were 0% fat, 4% BT, or 4% animal-vegetable oil blend (A-V); each fat treatment was fed with 0 or 7.5% forage. Across forage levels, the addition of fat increased (P < .01) ADG and G/F for cattle fed DRC. In Trial 3, 18 crossbred wether lambs (mean BW = 44.4 +/- 2.5 kg) were fed DRC and 7.5% forage and allotted randomly to the same fat treatments fed in Trial 2. Apparent total tract fat digestibility increased (P < .01) with the addition of BT or A-V. In Trial 4, 40 crossbred wethers (mean BW = 25 +/- 4.1 kg) and 16 ewes (mean BW = 23 +/- 2.7 kg) were individually fed 7.5% forage diets containing 0, 1, 2, or 4% BT. Addition of BT increased (linear, P = .10) G/F. In summary, fat addition to DRC finishing diets fed to yearling cattle did not consistently affect gain/feed, feed intake, and ADG.     

Lymphocyte beta -adrenoceptor downregulation in great danes with occult dilated cardiomyopathy (DCM) and with DCM and heart failure.

The importance of the adrenergic nervous system in supporting the failing heart has long been known. The adrenergic drive on cardiac structure and function has however some adverse effects, which include myocardial beta-adrenoceptor (beta-AR) downregulation and decreased beta-adrenergic responsiveness to cathecolamines. In dog lymphocytes, beta(1)-AR and beta(2)-AR populations are almost equally represented (with a slight prevalence of beta(2)) and a significant correlation between cardiac and lymphocytic adrenoceptors has been found. The aim of the present study was to investigate possible differences between the concentration of lymphocytic beta-AR in healthy dogs, dogs with dilated cardiomyopathy (DCM) and dogs with occult DCM. Three groups of great danes were considered: a control group (n =10), dogs with DCM (n =9) and dogs with occult DCM (n =4). Lymphocytic beta-AR populations were determined in all dogs. A substantial and significant decrease (P<0.05) in total-AR, beta(1)-AR and beta(2)-AR concentrations in the lymphocytes of dogs with symptomatic DCM and occult DCM compared to the control group was found. Although the mean value of the lymphocyte beta(1)-AR number in the asymptomatic group was double compared to the DCM group, this difference was not statistically significant. We conclude that in dogs beta-AR downregulation occurs early in the course of dilated cardiomyopathy. This finding may suggest the value of early use of a beta-blocker in the therapeutic regimen. Moreover, the continuous monitoring of lymphocytic beta-AR may represent a useful tool for the development of a more effective individual therapy.     

Effects of ractopamine on genetically obese and lean pigs

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

Beta 3-adrenergic agonist up-regulates uncoupling proteins 2 and 3 in skeletal muscle of the mouse

Chronic stimulation of the beta3-adrenergic receptor (AR) in obese animals resulted in a reduced adiposity associated with an increased expression of thermogenic uncoupling protein (UCP)1 in adipose tissues. In this study, the mRNA expression of newly cloned UCP isoforms (UCP2 and UCP3) were examined in obese yellow KK and C57BL control mice. UCP2 mRNA was found in all tissues examined, with higher levels in adipose tissues and skeletal muscle of the obese mice. UCP3 mRNA was expressed in skeletal muscle, heart and brown adipose tissue similarly in the two mouse strains. Daily injection of a selective beta3-adrenergic agonist, CL316,243 (0.1 mg/kg), for 10 days resulted in a marked reduction of white fat pad weight and 1.8-4.8-fold increase in the mRNA levels of UCP2 and UCP3 in skeletal muscle of obese mice. No noticeable change in the UCP2 and 3 mRNA levels was found in brown and white adipose tissues. It was also found that CL316,243 injection produced a marked and sustained elevation of the plasma free fatty acid level. These results, together with our previous findings of the fatty acid-induced UCP expression in a myocyte cell line in vitro, suggest that the beta3-AR agonist-induced UCP expression in skeletal muscle may be mediated through the elevated plasma free fatty acids. It was also suggested that anti-obesity effect of beta3-AR agonists is attributable to increased thermogenesis not only by UCP1 but also by UCP2 and UCP3.     

Binding of ractopamine HCl to ocular tissues of cattle and turkeys in vivo and to melanin in vitro

Experiments were conducted to determine the total residues remaining in ocular tissues of cattle and turkeys after oral administration of [14C]ractopamine HCl. Twelve cattle were intraruminally dosed with 0.9 mg x kg(-1) x d(-1) of [14C]ractopamine HCl for 7 d. Four cattle each were slaughtered with withdrawal periods of 48,96, and 144 h. Radioactive residues were not detectable in whole-eye homogenates from the cattle. Eight male and eight female turkeys per treatment received either 7.5, 22.5, or 30 ppm dietary [14C]ractopamine HCl (0.33, 1.02, and 1.36 mg x kg(-1) x d(-1); treatment groups 1, 2, and 3, respectively) for 7 d, and the birds were slaughtered with a 0-d withdrawal period. Eyes were dissected into retina/choroid/schlera (RCS), cornea/iris (CI), and aqueous humor (AH) fractions. Residues in RCS, CI, and AH of treatment 1 turkeys were not detectable. Residues in AH were < 0.02 ppm in treatment groups 2 and 3. Mean residues in RCS ranged from 0.15 to 0.26 ppm, and mean CI residues ranged from <0.09 to 0.17 ppm for treatment groups 2 and 3, respectively. The propensities of ractopamine and synthetic ractopamine metabolites to bind to melanin were studied in vitro using radiolabeled ligands with centrifugal filtration to separate melanin from unbound ligand. In vitro studies showed that [14C]ractopamine HCl binds to melanin rapidly and was displaced from melanin by other beta-agonists. Glucuronidation of ractopamine, which produced the major biotransformation product of ractopamine in all species studied to date, prevented binding to melanin. These studies demonstrate that the propensity for the in vivo binding of ractopamine HCl to pigmented ocular tissues is less than that reported for clenbuterol.     

Response to ractopamine-hydrogen chloride is similar in yearling steers across days on feed

Yearling steers (n = 2,552; 314 kg of initial BW) were used to evaluate the effects of ractopamine-HCl (RAC) and days on feed on performance, carcass characteristics, and skeletal muscle gene expression in finishing steers. Treatment groups included serial slaughter dates of 150, 171, or 192 d on feed. Within each slaughter date, steers either received RAC (200 mg/steer) daily for the final 28 d or were not fed RAC. All steers were initially implanted with Revalor-IS and were reimplanted with Revalor-S after 75 d on feed. At slaughter, muscle samples from the semimembranosus were collected for mRNA analysis of the beta-adrenergic receptors (beta-AR). Ractopamine administration increased (P < 0.05) ADG, G:F, and HCW and increased (P = 0.08) LM area. Ractopamine did not affect the dressing percentage, USDA yield grade, or quality grade (P > 0.3). There was no change in overall feed intake across the entire feeding period; however, feed intake was increased during the 28-d period during which the steers were fed RAC (P < or = 0.05). Greater days on feed decreased (P < 0.05) ADG, G:F, DMI, and the number of yield grade 1 and 2 carcasses. Also, greater days on feed increased (P < 0.05) HCW, dressing percentage, and the number of prime and choice carcasses, as well as the number of yield grade 4 and 5 carcasses. Increasing days on feed decreased (P < 0.05) the abundance of beta(1)-AR and beta(3)-AR mRNA and increased (P < 0.05) the abundance of beta(2)-AR mRNA in skeletal muscle samples obtained at slaughter. Ractopamine had no effect (P > 0.10) on the abundance of beta(1)-AR or beta(3)-AR mRNA, but tended (P = 0.09) to increase beta(2)-AR mRNA. Additional time-course studies with primary muscle cell cultures revealed that advancing time in culture increased (P < 0.001) beta(2)-AR mRNA but had no effect (P > 0.10) on beta(1)-AR or beta(3)-AR mRNA. We conclude that days on feed and RAC are affecting beta-AR mRNA levels, which could, in turn, impact the biological response to RAC feeding in yearling steers.     

Differential effects of dexamethasone and clenbuterol on rat growth and on beta2-adrenoceptors in lung and skeletal muscle

Beta-adrenergic agonists increase growth rate, but their efficacy is reduced over time as the number of beta2-adrenoceptors in muscle decreases. Dexamethasone increases beta2-adrenoceptor density in many tissues, but this effect has not been reported in skeletal muscle. In this study, male rats were treated daily for 10 d with either clenbuterol (4 mg/kg of feed), dexamethasone (.2 mg/kg BW, s.c.), or clenbuterol plus dexamethasone. Untreated rats served as controls. Dexamethasone caused a marked suppression of growth rate, which resulted in decreased (P < .001) body weight (-29%), carcass weight (-30%), hind-limb muscles (-22%), omental fat (-22%), and heart weight (-10%). Feed intake was reduced (-26%), but feed conversion efficiency was also impaired (P < .001). Clenbuterol caused a small increase in growth rate (+6%; P < .05), with an increase in leg muscle (+7%; P < .01) and heart mass (+8%; P < .05). Feed efficiency was improved (P < .001) by clenbuterol. Rats given the combined treatment still showed a reduction in growth rate (-81%). Clenbuterol caused only a mild attenuation of the effects of dexamethasone on feed intake, BW, and carcass weight, but reduced the catabolic effect of dexamethasone on hind-limb muscle to only -8%. Clenbuterol caused a slight increase in the affinity beta2-adrenoceptors in lung for binding to the radioligand (-)[125I]iodocyanopindolol. Relative to control values, the density of beta2-adrenoceptors in lung was +31% with dexamethasone treatment, -45% with clenbuterol, and -23% with the combined treatment. Clenbuterol also decreased beta2-adrenoceptors in skeletal muscle (-35%), but so did dexamethasone (-13%), so the effects of the beta-adrenergic agonist were not attenuated through use of the combined treatment (-40%). The results show that the inductive effect of glucocorticoids on beta2-adrenoceptors is tissue-specific and that glucocorticoid treatment is not a useful adjunct to beta-adrenergic agonist treatment in animal production.     

Response of barrows to space allocation and ractopamine

An experiment using 264 crossbred barrows was conducted to examine the interaction between space allocation and dietary ractopamine addition on pig performance and carcass characteristics using a 2 x 2 factorial arrangement of treatments. Treatments were 0.55 (19 pigs per pen) or 0.74 (14 pigs per pen) m2/pig from start (29.7 +/- 0.1 kg BW) to slaughter (108 kg BW) in a fully slatted facility and 0 or 10 ppm (as-fed basis) ractopamine for 28 d before slaughter. There were few treatment interactions. Pigs given 0.55 m2/pig had a lower ADG (P = 0.010), ADFI (P = 0.088), 10th-rib backfat depth on d 86 (P = 0.010), and carcass loin muscle depth (P = 0.011) than pigs given 0.74 m2/pig. There was no difference in feed conversion (P = 0.210) as a result of space allocation. Pigs fed diets containing 10 ppm ractopamine had decreased (P = 0.004) ADFI and improved (P = 0.001) feed conversion efficiencies for the 28-d feeding period, along with greater loin depth (P = 0.005) and carcass lean percent (P = 0.001). The improvements in 28-d carcass lean growth associated with feeding 10 ppm ractopamine resulted in an improvement in overall daily fat-free lean gain (P = 0.046). Under these experimental conditions, the response to dietary ractopamine was similar for crowded and uncrowded pigs.     

Interactive effect of ractopamine and dietary fat source on quality characteristics of fresh pork bellies

Crossbred pigs (n = 216) were used to test the interaction, if any, of ractopamine (RAC) and dietary fat source on the characteristics of fresh pork bellies. Pigs were blocked by BW (77.6 +/- 6.5 kg) and allotted randomly to pens (6 pigs/pen). After receiving a common diet devoid of RAC for 2 wk, pens within blocks were assigned randomly to 1 of 4 treatments arranged in a 2 x 2 factorial design, with 5% fat (beef tallow vs. soybean oil) and RAC (0 vs. 10 mg/kg). At the conclusion of the 35-d feeding period, pigs were slaughtered at a commercial pork packing plant (average BW of 108.8 +/- 0.6 kg), and fresh bellies were captured during carcass fabrication. Neither RAC (P = 0.362) nor fat source (P = 0.247) affected belly thickness. Subjective (bar-suspension) or objective (compression test) measures of belly firmness were not (P > or = 0.148) affected by the inclusion of RAC in the diet; however, bellies from pigs fed soybean oil (SBO) were softer than those from pigs fed beef tallow (BT), as indicated by perpendicular (P < or = 0.005) and parallel (P < 0.001) suspensions. Moreover, bellies from BT-fed pigs required more (P = 0.096) force to compress 50% of their thickness than bellies from SBO-fed pigs (52.29 vs. 43.51 kg). Color (L*, a*, and b* values) of the belly lean and fat was not (P > or = 0.131) affected by RAC, and lean color was similar (P > or = 0.262) between fat sources; however, belly fat from BT-fed pigs was lighter (P = 0.030) and redder (P = 0.013) in color than belly fat from SBO-fed pigs. Bellies of SBO-fed pigs had greater (P < 0.001) proportions of PUFA and lower (P < 0.001) proportions of SFA and MUFA than belly fat from pigs fed BT. Regardless of the RAC inclusion level, PUFA:SFA and iodine values were lower in belly fat from pigs fed BT than SBO; however, within SBO-fed pigs, PUFA:SFA and iodine values were further increased by feeding RAC (RAC x fat source, P < 0.001). As expected, dietary fat source altered the fatty acid composition of fresh pork bellies, which subsequently impacted fresh belly firmness. Interestingly, including RAC in swine finishing diets exacerbated the effect of feeding SBO on pork fat polyunsaturation.     

Mepartricin long-term administration regulates steroid hormone and adrenergic receptor concentrations in the prostate of aged rats

Mepartricin is a semi-synthetic macrolide antibiotic developed as a drug for the treatment of benign prostatic hyperplasia (BPH) in human patients. In the present study, aged rats are used as an experimental model to evaluate the effects of mepartricin on circulating hormone concentrations and prostate receptor concentrations, to compare these possible effects with clinical findings observed in long-term treated dogs. Fifty-six aged male rats were randomly divided into four experimental groups treated orally with 0 (group 1), 2 mg (group 2), 5 mg (group 3) and 20 mg (group 4) mepartricin/kg of body weight. for 28 days respectively. Serum oestradiol and testosterone concentrations were measured by radio-immune-assays methods. Binding assays were used to measure the prostate concentrations of oestrogen receptors (ER), androgen receptors (AnR), alpha(1)-adrenergic receptor (alpha(1)-AR), and beta-adrenerergic receptor (beta-AR) subtypes. Mepartricin induced a significant reduction of prostate weight and serum oestradiol concentrations. Serum testosterone concentrations were unaffected. The treatment induced a significant down-regulation of ER concentrations (P < 0.05) and a significant up-regulation of AnR (P < 0.05) in rat prostate. Mepartricin induced a significant (P < 0.05) dose-dependent up-regulation of alpha(1)-AR and beta(2)-AR. In contrast, the concentration of beta(3)-ARs was significantly decreased (P < 0.05) in treated animals. The increase in prostate beta(2)-AR concentrations observed in subjects treated with mepartricin may be a favourable element in the evolution of BPH, because of the role exerted by these receptors in the control of prostatic smooth muscle relaxation. Curiously, beta(3)-AR concentrations were significantly reduced in treated animals. Data collected suggest that the prostatic beta-AR expression might be strongly influenced by oestrogen deprivation (mepartricin treatment); therefore, the combination of oestrogen suppression (mepartricin) and adrenergic suppression (alpha(1)-AR blockers) may be proposed as a possible nonhormonal therapeutic strategy for the treatment of benign prostatic hyperplasia in dogs.     

Conjugated linoleic acid content in adipose tissue of calves suckling beef cows on pasture and supplemented with raw or extruded soybeans

The concentration of CLA in adipose tissue can be increased in ruminants by feeding pasture and extruded soybeans. The objective of this study was to evaluate maternal supplementation of raw (RS) or extruded (ES) soybeans on the concentrations of CLA in milk fat of cows and s.c. adipose tissue of suckling calves. Thirty-two spring-calving cows (BW 624 +/- 76 kg; BCS 3.5 +/- 0.4; mean +/- SD) and calves (BW 127 +/- 15 kg) were separated into 2 groups. Cows were distributed to have 8 calves of each sex in both groups. When animals were turned out to pasture, dams received 2 kg/d of either RS or ES. Dietary treatments had no effect on average milk intake (P = 0.22) and pasture forage intake (P = 0.13) for calves over the course of the grazing season. As a result, no effect of treatments was observed on ADG (P = 0.26). At weaning, milk fat content of CLA reached 15.4 and 24.2 mg/g of total fatty acids for cows fed RS and ES, respectively (P = 0.02). The CLA concentrations in adipose tissue were 16.9 and 25.0 mg/g of total fatty acids for calves suckling dams fed RS and ES, respectively (P < 0.001). Overall, results demonstrated supplementing grazing cows with ES increased CLA content in milk and adipose tissue of suckling calves.     

不同β-受体激动剂添加模式对肉牛血液生化指标和激素水平的影响

试验旨在研究不同β-受体激动剂添加模式对肉牛血液生化指标和激素水平的影响。选取15头体况良好、体重相近（257.9 kg±33.3 kg）的西门塔尔肉牛,随机分为3组,每组5头。对照组饲喂基础日粮;试验Ⅰ组添加莱克多巴胺,添加剂量为670.0 μg/kg体重;试验Ⅱ组添加莱克多巴胺、沙丁胺醇和克伦特罗的混合物,添加剂量分别为223.3、50.0、5.3 μg/kg体重。给药期28 d,停药期28 d。结果表明,与对照组相比,在给药第28天时,试验Ⅰ组肉牛血浆中游离脂肪酸（FFA）浓度显著降低（P<0.05）,试验Ⅱ组肉牛血浆中葡萄糖（GLU）和游离脂肪酸浓度均显著降低（P<0.05）;整个试验过程中,除停药第28天时试验Ⅰ组肉牛血浆中胰岛素（INS）水平显著高于对照组外（P<0.05）,β-受体激动剂对各试验组血浆中激素水平均无显著影响（P>0.05）。综合上述试验结果,肉牛血浆中的FFA可作为β-受体激动剂潜在的生物标志物,可通过对其的监测来监管β-受体激动剂在肉牛生产环节中的非法使用。     

Manipulation of growth in pigs through treatment of the neonate with clenbuterol and somatotropin

Neonatal pigs were treated with lipolytic agents to determine whether this would cause a long-term decrease in their ability to deposit fat, with a consequent increase in muscle growth and feed efficiency. Groups of 25 female piglets were given clenbuterol (100 microg/kg BW), porcine somatotropin (pST; 100 microg/kg BW), pST plus clenbuterol, or saline injections from 3 d to 40 d of age. Five piglets from each group were then slaughtered to determine body composition. Clenbuterol and pST both increased ADG up to weaning when given separately (24%, P < 0.05; 20%, P < 0.1 respectively) but did not reduce fat deposition. In contrast, pigs given clenbuterol plus pST showed no increase in ADG and a 41% reduction in carcass fat (P < 0.05). Clenbuterol caused a marked decrease in beta2-adrenoceptor density in porcine adipose tissue (P < 0.001) and skeletal muscle (P < 0.01). This effect was attenuated by concurrent pST treatment, which helps to explain the synergistic effect of these drugs on fat deposition. Once the drugs were withdrawn at 40 d, the anabolic effect of pST gradually disappeared, so that the live weight of pST-treated and control pigs was identical at 168 d. Clenbuterol withdrawal caused the rapid loss of extra weight gained, plus an additional 4 to 5 kg live weight that was never recovered. During the 4-wk finishing period there was an increase in feed intake in pigs that had previously undergone treatment with pST (23%, P < 0.1), with no increase in ADG, and so feed efficiency was impaired (P < 0.05). Pigs that were treated with pST plus clenbuterol showed no marked increase in feed intake during this period. Carcasses from clenbuterol-treated pigs tended to be leaner at 168 d, but there was no long-term effect of pST or the combined treatment on carcass composition. Overall, the treatment of neonatal pigs with repartitioning agents was counter-productive, due to the withdrawal effects of the beta-adrenefgic agonist and the delayed long-term effect of pST on feed intake.     

Effect of feedlot management system on response to ractopamine-HCl in yearling steers

Two experiments evaluated the effects of conventional and natural feedlot management systems (MS) on ractopamine-HCl (RAC) response in yearling steers. Feedlot performance, carcass characteristics, skeletal muscle gene expression, and circulating IGF-I concentrations were measured. The conventional system included a combined trenbolone acetate and estradiol implant, Revalor-S (IMP), as well as monensin-tylosin feed additives (IA). Treatments were arranged in a 2 x 2 factorial and included: 1) natural (NAT): no IMP-no IA, no RAC; 2) natural plus (NAT+): no IMP-no IA, RAC; 3) conventional (CON): IMP-IA, no RAC; and 4) conventional plus (CON+): IMP-IA, RAC. In Exp. 1, one hundred twenty crossbred steers (initial BW = 400 +/- 26 kg) were allotted randomly to treatment in a randomized complete block design (BW was blocking criteria); pen was the experimental unit. In Exp. 2, twenty-four individually fed crossbred steers (initial BW = 452 +/- 25 kg) were used in a randomized complete block design (BW was blocking criteria) and assigned to the same treatments as Exp. 1, with 6 steers/treatment. In Exp. 2, serum was harvested on d 0 and 31 and within the 28-d RAC feeding period, at d 0, 14, and 28. Longissimus biopsy samples were taken on d 0, 14, and 28 of the RAC feeding period for mRNA analysis of beta-adrenergic receptors and steady-state IGF-I mRNA. In Exp. 1, ADG, G:F, final BW, and HCW were greatest for CON+ (P < 0.01). During the final 37 d, RAC increased ADG (P = 0.05) and increased overall G:F (P = 0.02). Marbling score was reduced (P = 0.02), and yield grade was improved with RAC (P = 0.02), but RAC did not affect dressing percentage (P = 0.96) or HCW (P = 0.31). In Exp. 2, MS x RAC interactions were detected in ADG and G:F the last 28 d, overall ADG and overall G:F, final BW, and HCW (P < 0.01). Dressing percentage, yield grade, and marbling score were not altered by MS or RAC (P > 0.10). Circulating IGF-I concentration was increased on d 31 by the conventional MS, and concentration was greater throughout the study than NAT steers (P < 0.01). Circulating IGF-I concentrations were not changed by RAC (P = 0.49). Abundance of beta(1)-AR mRNA tended to increase (P = 0.09) with RAC, but RAC did not affect beta(2)-AR, beta(3)-AR, or IGF-I mRNA (P > 0.40). Management system did not affect beta(1)-AR, beta(2)-AR, beta(3)-AR, or IGF-I mRNA (P > 0.18), yet a trend (P = 0.06) for MS x RAC for beta(2)-AR mRNA was detected. These results indicate that response to RAC is affected by feedlot management practices.