Quantitative modification of the testicular structure in pigs fed with anabolic doses of clenbuterol

Morphological and structural data of the testes of thirty male pigs were recorded in order to evaluate the effects of an anabolic clenbuterol treatment. Pigs aged 6 months were randomly allocated to one of three experimental groups. In two treated groups, the animals were fed with anabolic doses of clenbuterol (1 ppm); in the CLB group (n = 10) clenbuterol was given until they were slaughtered (treatment period = 3 months) whereas in the CLBW group (n = 10) the clenbuterol was withdrawn two weeks before slaughter (treatment period = 2.5 months); clenbuterol was not given to the pigs of the control group (n = 10). Stereological estimations of the tissular volume fraction and tubular volume density were applied to quantify the structural constituents of the testes. The results showed an increased volume fraction of the testicular interstitium especially in the Leydig cell population, as a result of the clenbuterol treatment. The increase in the nuclear volume fraction of the Leydig cells was the more persistent change in the variations recorded in both treated groups with respect to the control. A regression of the seminal epithelium was also recorded in the treated animals. The rest of the structural parameters were closer to the normal figures in the CLBW group, suggesting a recovery of the testicular structure when clenbuterol was withdrawn.     

Morphological and quantitative study of the Leydig cells of pigs fed with anabolic doses of clenbuterol

The effects of clenbuterol administered at anabolic doses on the testicular interstitium were studied in 30 pigs allocated to three experimental groups. The diet of two groups was supplemented with clenbuterol (Clb) (1 ppm), but whereas in the Clb+ group the treatment was given until slaughter (treatment period: 3 months), in the Clb- group the clenbuterol was withdrawn 2 weeks before slaughter (treatment period: 2-5 months); in the control group, the pigs were fed without clenbuterol. For histological procedures, a fractional sampling scheme was applied and routine techniques for light and transmission electron microscopy were used. The results of subjective morphology and morphometrics showed slight differences between the treated and the control groups. Conversely, the stereological results identified a prominent hyperplasia of the Leydig cells and ultrastructural analysis of these cells revealed a conspicuous increase in the organelles related to testosterone production, suggesting a functional activation of the interstitial cells in response to the clenbuterol treatment.     

beta-Adrenergic receptor agonists increase apoptosis of adipose tissue in mice

beta-Adrenergic receptor (beta-AR) agonists increase muscle mass and decrease body fat in rodents and livestock. With oral administration, however, the effects of beta1-AR and beta2-AR can be different, depending on the species tested. We tested the effects of clenbuterol, a beta2-AR agonist, and ractopamine, a beta1/beta2-AR agonist, on growth, adiposity and adipose tissue apoptosis in male and female mice by feeding diets containing control, 200 ppm clenbuterol, or 200 or 800 ppm ractopamine. Food intake (FI) was measured daily; body weight (BW) and temperatures (BT) were measured on days 0, 3, 7, 10, 14, 17, and 20. On day 21 mice were sacrificed, body composition was determined using PIXImus densitometry, and muscle and adipose tissues were collected. There were no treatment effects on BT, FI, BW, feed efficiency or body composition. Retroperitoneal (Rp) and epididymal/parametrial (Epi/Par) fat pad masses were reduced in both 800 ppm ractopamine (40+/-3mg and 207+/-20mg, respectively) and clenbuterol (35+/-7 mg and 211+/-22 mg) treated mice compared to control (66+/-8 mg and 319+/-30 mg, P<0.05). Brown adipose tissue (BAT) mass was greater (P<0.05) in clenbuterol treated mice compared to other treatments. Adipose tissue apoptosis (% DNA fragmentation) was increased in Epi/Par fat pads in clenbuterol (5.2+/-1.1%) and 800 ppm ractopamine (4.1+/-0.8%) treated mice compared to control (1.7+/-0.4%, P<0.05). These findings show that WAT apoptosis can be induced by activation of beta-AR in mice, although the mechanism is unknown.     

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.     

Ghrelin对雌激素诱导小鼠胸腺细胞凋亡的抑制作用

6周龄BALB/c雌性小鼠80只,分为4组：雌激素＋Ghrelin组、雌激素＋生理盐水组、生理盐水组、空白对照组。雌激素＋Ghrelin组首先隔日腹腔注射苯甲酸雌二醇（0.1mg/只）2周,然后采用相同方法注射Ghrelin（120μg/只）2周;雌激素＋生理盐水组首先注射苯甲酸雌二醇2周,然后注射生理盐水2周;生理盐水组注射生理盐水4周;空白对照组不注射任何试剂。测量各组小鼠的胸腺指数,同时应用光镜、电镜和流式细胞术检测胸腺的显微结构、超微结构和胸腺细胞凋亡率。结果雌激素＋Ghrelin组的胸腺指数极显著大于雌激素＋生理盐水组,胸腺细胞凋亡率极显著小于雌激素＋生理盐水组（P〈0.01）,而二者与生理盐水组和空白对照组均差异不显著（P〉0.05）;雌激素＋Ghrelin组的胸腺显微结构和超微结构基本恢复正常,并与生理盐水组和空白对照组相似。结论得出Ghrelin可以通过抑制胸腺细胞凋亡和促进胸腺细胞增殖,从而逆转雌激素诱导的小鼠胸腺萎缩。     

Stereological study of the adrenal gland of calves treated with clenbuterol

Stereological methods were used to investigate the morphometric variations in the adrenal cell population of calves dosed orally with clenbuterol at an anabolic dose of 20 microg/kg bodyweight per day for 12 weeks. In the treated group the size of the nuclei increased with respect to the control group, and the increases were significant for the maximum linear parameters in all the regions except the zona fasciculata. The largest increases were observed in the epinephrine-producing cells. The quantitative stereological data showed highly significant increases in the nuclear volume fraction, the nuclear surface density and the numerical density in the zona fasciculata of the treated group.     

CXCL8((3-73))K11R/G31P antagonizes the neutrophil chemoattractants present in pasteurellosis and mastitis lesions and abrogates neutrophil influx into intradermal endotoxin challenge sites in vivo

Toxic products such as reactive oxygen intermediates released by activated polymorphonuclear neutrophil (PMN) have an important role in the pathophysiology of diseases associated with the deposition of immune complexes (IC) in tissues. IC-induced activation of PMN requires adhesion mediated by integrin adhesion receptors. Of the integrins expressed on PMN, the beta(2) family has been found to be of particular importance for activation of PMN by IC. beta(2) Integrin ligand binding must be activated to enable adhesion to IC. Both activating and inhibitory signals regulate beta(2) integrin ligand avidity and adhesion. The second messenger cyclic adenosine monophosphate (cAMP) has been demonstrated to inhibit the activation of PMN in response to a variety of stimuli. The purpose of this study is to test the hypothesis that cAMP-dependent signals inhibit beta(2) integrin-dependent adhesion of equine PMN to immobilized IC and subsequent adhesion-dependent activation of respiratory burst activity. Treatment of equine PMN with beta(2) adrenergic agonists isoproterenol or clenbuterol, which trigger an increase in intracellular cAMP concentration, inhibited adhesion of equine PMN to IC in a dose dependent manner. Similarly, inhibition of cAMP hydrolysis by the non-specific phosphodiesterase (PDE) inhibitor pentoxifylline and the PDE 4-specific inhibitor rolipram inhibited adhesion of equine PMN to IC. Elevation of intracellular cAMP levels with pentoxifylline, clenbuterol and rolipram also inhibited IC-induced activation of respiratory burst activity in equine PMN. Importantly, co-treatment of equine PMN with rolipram and either beta(2) adrenergic agonist synergistically inhibited both the adhesion of equine PMN to IC as well as the subsequent respiratory burst activity.     

Effects of adrenergic agonists and antagonists on the blood pressure and heart rate of the pig fetus

The effects of adrenergic agonists and antagonists on blood pressure and heart rate were investigated in 18 chronically catheterised pig fetuses aged between 102 and 109 days of gestation (term is 114 days). One fetus had been decapitated in utero at 42 days of gestation. The alpha adrenergic agonist methoxamine produced a small but dose dependent hypertension and a dose related slowing in heart rate. The beta adrenergic agonist isoprenaline decreased mean arterial pressure in a dose related manner and produced tachycardia. Propranolol, a beta adrenergic blocker, increased mean arterial pressure and decreased heart rate. The response to subsequent alpha adrenergic blockade with phentolamine was hypotension and a slight bradycardia. Decapitation at 42 days of gestation did not seem to change the fetal responsiveness to adrenergic agonists but removed the blood pressure response to beta blockade. These observations indicate that the heart and circulation of the pig fetus are under adrenergic vasomotor control during late gestation.     

Acute and Subacute Metabolic and Endocrine Effects of Clenbuterol in Female Pigs

The aim of the study was to assess the relationship between acute and subacute metabolic and endocrine effects after intravenous administration of the ₂-adrenergic agonist clenbuterol in a growth-promoting dose to female pigs. Acute metabolic and endocrine effects were assessed by measuring the blood glucose, serum insulin and nonesterified fatty acid (NEFA) concentrations during 300 min after a single administration of clenbuterol. Significantly higher serum insulin and NEFA concentrations (19.90±2.50 U/ml, p<0.01, and 0.69±0.04 mmol/L, p<0.001, respectively) were measured 30 min after the preprandial administration of clenbuterol in female pigs. Over the same period, the levels of blood glucose (4.42±0.30 mmol/L) showed no difference from those of control pigs. The postprandial serum NEFA concentration decreased moderately during 210 min after feeding. Postprandial blood glucose and insulin concentrations increased and reached maximal levels 120 min after clenbuterol administration (10.91±0.60 mmol/L and 85.22±7.24 U/ml, respectively), and returned to basal levels at 300 min (4.20±0.21 mmol/L and 7.75±1.60 U/ml, respectively) after the administration of clenbuterol. Subacute metabolic and endocrine effects were assessed by measuring the blood glucose, serum insulin and NEFA concentrations for 21 days after the repeated doses of clenbuterol. In addition, the influence of clenbuterol administration on the endocrine regulation of the onset of the next expected oestrus in female pigs was assessed by measuring their serum 17-oestradiol and progesterone concentrations. Blood glucose, serum insulin and NEFA concentrations after the last administration of clenbuterol did not differ significantly from those in control animals. The onset of the next expected oestrus occurred regularly without any significant difference in serum 17-oestradiol or progesterone concentrations between the treated (9.83±2.60 pg/ml and 0.15±0.03 ng/ml) and control pigs (8.52±2.70 pg/ml and 0.25±0.06 ng/ml). The study results suggest the duration of intravenous administration of clenbuterol in a growth-promoting dose necessary to influence the metabolic and endocrine activities in female pigs.     

Testicular damage from anabolic treatments with the beta(2)-adrenergic agonist clenbuterol in pigs: a light and electron microscope study

The morphological consequences of anabolic clenbuterol treatment on the testicular parenchyma were investigated in 30 pigs at morphological and ultrastructural levels. Clenbuterol was given with food (1 ppm). In the first group (n=10), treatment was maintained until slaughter (experimental period 3 months). In the second group (n=10), clenbuterol was withdrawn 2 weeks before slaughter (experimental period 2.5 months). A third group (n=10) of pigs not fed with clenbuterol served as controls. Animals were slaughtered at 9 months of age and samples of testicular parenchyma were collected for light and electron microscope studies. In the clenbuterol-treated groups, the interstitial cells showed a considerable increase in the organelles involved in testosterone production, with an increased development of the mitochondria, smooth endoplasmic reticulum, Golgi apparatus and lipid droplets compared to the control group. The seminal epithelium displayed many lipid vacuoles and evident signs of tubular involution, such as degenerating and multinucleate germ cells. Sertoli cells gave evidence of metabolic alterations such as large lipid deposits and cytolysosomes.     

Testicular Damage from Anabolic Treatments with the β2-Adrenergic Agonist Clenbuterol in Pigs: A Light and Electron Microscope Study

The morphological consequences of anabolic clenbuterol treatment on the testicular parenchyma were investigated in 30 pigs at morphological and ultrastructural levels. Clenbuterol was given with food (1 ppm). In the first group (n=10), treatment was maintained until slaughter (experimental period 3 months). In the second group (n=10), clenbuterol was withdrawn 2 weeks before slaughter (experimental period 2.5 months). A third group (n=10) of pigs not fed with clenbuterol served as controls. Animals were slaughtered at 9 months of age and samples of testicular parenchyma were collected for light and electron microscope studies. In the clenbuterol-treated groups, the interstitial cells showed a considerable increase in the organelles involved in testosterone production, with an increased development of the mitochondria, smooth endoplasmic reticulum, Golgi apparatus and lipid droplets compared to the control group. The seminal epithelium displayed many lipid vacuoles and evident signs of tubular involution, such as degenerating and multinucleate germ cells. Sertoli cells gave evidence of metabolic alterations such as large lipid deposits and cytolysosomes.     

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.     

雌激素诱导小鼠胸腺萎缩过程中细胞因子及凋亡相关蛋白基因表达的变化

本试验应用光镜、电镜、流式细胞术、实时定量PCR技术研究了雌激素诱导小鼠胸腺萎缩过程中胸腺指数、胸腺显微和超微结构、胸腺细胞凋亡率及部分细胞因子和凋亡相关蛋白基因表达的变化。结果注射雌激素后,小鼠胸腺指数显著下降,胸腺中凋亡细胞数量显著上升,细胞因子TGF-β1表达量显著升高,IL-6表达量略为升高,而IL-7表达量显著降低;凋亡相关蛋白Caspase-3、Caspase-9、FADD表达量显著上升,FasL表达量略有上升,而Bcl-2表达量显著降低。表明雌激素可能一方面通过调节胸腺细胞因子抑制胸腺上皮细胞的增殖,另一方面通过激活Caspase级联程序的启动和执行阶段及Fas/FasL凋亡信号通路促进胸腺细胞的凋亡,从而诱导小鼠胸腺萎缩。     

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.     

Ghrelin对雌激素诱导小鼠胸腺萎缩过程中细胞因子及凋亡相关蛋白基因表达的影响

应用光镜和实时定量PCR技术研究了Ghrelin对雌激素诱导小鼠胸腺萎缩过程中胸腺形态学以及部分细胞因子和凋亡相关蛋白基因表达的影响。结果显示,注射Ghrelin后,雌激素诱导的小鼠萎缩胸腺在形态学上基本恢复到正常水平,胸腺中IL-6、TGF-[31、Caspase3、FADDmRNA含量显著降低,Caspase9、FasLmRNA含量略为下降,而IL-7、Bcl-2mRNA含量有所上升。结果表明,Ghrelin可能通过促进胸腺上皮细胞的增殖以及阻断Caspase级联程序和Fas／FasL凋亡信号通路抑制胸腺细胞的凋亡,从而逆转雌激素诱导的小鼠胸腺萎缩。     

Use of a beta 2-adrenergic stimulant (clenbuterol) for eliminating night-time calving.

To determine whether beta 2-adrenergic stimulant (clenbuterol) would exhibit beneficial effects upon the elimination of night-time calving, 42 Holstein Friesian cows and heifers at the first stage of labour were injected intramuscularly twice with clenbuterol; 300 micrograms at 18:00 and 210 micrograms at 22:00. Other 26 cows and heifers of the same breed at the first stage of labour at 18:00 were not treated and served as controls. All of the treated animals, but one, calved after 5:00 in the next morning, showing a peak of parturition between 5:00 and 10:00. In contrast to this, 42% of the control animals calved at night between 22:00 and 5:00. Thus, the double administrations of clenbuterol were shown to be effective for eliminating night-time calving. The cows treated with clenbuterol tended to show lower incidences of dystocia and retained placenta and a higher first insemination conception rate than the control animals. No adverse effects of the treatment on the viability of newborn calves and milk yields were observed.     

Effect of dietary clenbuterol and cimaterol on muscle composition, beta-adrenergic and androgen receptor concentrations in broiler chickens

Illegal dietary supplementation with beta(2)-agonists has been shown to increase protein deposition and decrease fat accretion in domestic animals. In poultry the metabolic and endocrine responses to beta(2)-agonists are not fully elucidated. In this trial the effects of dietary clenbuterol (1 p.p.m.) and cimaterol (1 p.p.m.) on muscle composition and endocrine response of male broiler chickens were studied. Dietary clenbuterol induced a slight, but in general not significant, improvement of zootechnical performances and carcass yields. Chemical composition of muscle was not influenced by dietary treatments, even if a slight improvement of protein content was observed in treated groups. No effects on fatty acid composition of meat were detected. Both clenbuterol and cimaterol treatments caused a downregulation in testicular androgen receptors and in pulmonary, cardiac and central nervous system beta-adrenergic receptors.     

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.     

Beta-adrenergic receptor activity in ponies with recurrent obstructive pulmonary disease.

Pulmonary function measurements were made in control ponies and in ponies with recurrent obstructive pulmonary disease (principals) during clinical remission and during an attack of acute airway obstruction. The ponies were given beta-adrenergic antagonists and agonists to determine the role of beta receptors in recurrent obstructive pulmonary disease, and to determine the subtypes of beta receptors mediating bronchodilation in ponies. Aerosol administration of the beta antagonists, propranolol (beta 1 and beta 2), atenolol (beta 1), and butoxamine (beta 2) decreased dynamic compliance (Cdyn) and increased pulmonary resistance (RL) in the principal ponies during airway obstruction, but were without effect when the ponies were in clinical remission. Intravenous administration of atropine reversed the effect of atenolol on Cdyn and RL, but was without effect on the decrease in Cdyn and increase in RL observed after butoxamine administration. The beta antagonists did not affect airway function in the control ponies. The effect of beta blockade on Cdyn and RL suggests beta-adrenergic activation in the central and peripheral airways of principal ponies, mediated through both beta 2- and beta 1-adrenergic receptors. The aerosol beta agonists, isoproterenol (beta 1 and beta 2), and clenbuterol (beta 2) attenuated histamine-induced airway obstruction to a similar extent in control ponies that were given histamine IV. In addition, the beta 1 antagonist, atenolol, did not attenuate the bronchodilation observed with isoproterenol. We concluded that, although beta 1- and beta 2-adrenergic receptors exist in pony airways and are activated during acute airway obstruction, bronchodilation in response to beta agonists in ponies seems to be mediated primarily by beta 2-adrenergic receptors.     

β-激动剂对鸭Ca、Mn、Zn代谢的影响

用芬茗和克仑特罗饲喂肉鸭２１ｄ,二者对鸭生产性能的影响基本一致。此时,鸭血清碱性磷酸酶（ＡＫＰ）活性和肌浆Ｃａ含量明显增高,而血清和肌浆Ｍｎ含量明显减少。在相同日粮条件下,芬茗处理鸭肌浆Ｃａ、Ｍｎ、Ｚｎ含量均高于克仑特罗处理者（Ｃａ、Ｍｎ达到Ｐ＜０．０５）。克仑特罗处理后引起鸭体内Ｍｎ、Ｚｎ元素丢失增加,这可能是畜禽的后肢乏力、跛行和蹄裂的原因之一。