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Lynch, Gordon S., Alan Hayes, Siun P. Campbell, and David A. Williams. "Effects of β2-agonist administration and exercise on contractile activation of skeletal muscle fibers." Journal of Applied Physiology 81, no. 4 (October 1, 1996): 1610–18. http://dx.doi.org/10.1152/jappl.1996.81.4.1610.
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Lynch, Gordon S., Alan Hayes, Siun P. Campbell, and David A. Williams. Effects of β2-agonist administration and exercise on contractile activation of skeletal muscle fibers. J. Appl. Physiol. 81(4): 1610–1618, 1996.—Clenbuterol, a β2-adrenoceptor agonist, has therapeutic potential for the treatment of muscle-wasting diseases, yet its effects, especially at the single-fiber level, have not been fully characterized. Male C57BL/10 mice were allocated to three groups: Control-Treated mice were administered clenbuterol (2 mg ⋅ kg−1 ⋅ day−1) via their drinking water for 15 wk; Trained-Treated mice underwent low-intensity training (unweighted swimming, 5 days/wk, 1 h/day) in addition to receiving clenbuterol; and Control mice were sedentary and untreated. Contractile characteristics were determined on membrane-permeabilized fibers from the extensor digitorum longus (EDL) and soleus muscles. Fast fibers from the EDL and soleus muscles of Treated mice exhibited decreases in Ca2+ sensitivity. Endurance exercise offset clenbuterol’s effects, demonstrated by similar Ca2+ sensitivities in the Trained-Treated and Control groups. Long-term clenbuterol treatment did not affect the normalized maximal tension of fast or slow fibers but increased the proportion of fast fibers in the soleus muscle. Training increased the proportion of fibers with high and intermediate succinate dehydrogenase activity in the EDL and soleus muscles, respectively. If clenbuterol is to be used for treating muscle-wasting disorders, some form of low-intensity exercise might be encouraged such that potentially deleterious slow-to-fast fiber type transformations are minimized. Indeed, in the mouse, low-intensity exercise appears to prevent these effects.
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&NA;. "Clenbuterol." Reactions Weekly &NA;, no. 374 (October 1991): 4. http://dx.doi.org/10.2165/00128415-199103740-00014.
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&NA;. "Clenbuterol." Reactions Weekly &NA;, no. 1082 (December 2005): 10. http://dx.doi.org/10.2165/00128415-200510820-00026.
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&NA;. "Clenbuterol." Reactions Weekly &NA;, no. 1242 (March 2009): 16–17. http://dx.doi.org/10.2165/00128415-200912420-00046.
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&NA;. "Clenbuterol." Reactions Weekly &NA;, no. 1327 (November 2010): 13. http://dx.doi.org/10.2165/00128415-201013270-00039.
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PRATHER, IRVINE D., DAVID E. BROWN, PERRY NORTH, and JUDY R. WILSON. "Clenbuterol." Medicine & Science in Sports & Exercise 27, no. 8 (August 1995): 1118???1121. http://dx.doi.org/10.1249/00005768-199508000-00003.
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Kline, William O., Frank J. Panaro, Hayung Yang, and Sue C. Bodine. "Rapamycin inhibits the growth and muscle-sparing effects of clenbuterol." Journal of Applied Physiology 102, no. 2 (February 2007): 740–47. http://dx.doi.org/10.1152/japplphysiol.00873.2006.
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Clenbuterol and other β2-adrenergic agonists are effective at inducing muscle growth and attenuating muscle atrophy through unknown mechanisms. This study tested the hypothesis that clenbuterol-induced growth and muscle sparing is mediated through the activation of Akt and mammalian target of rapamycin (mTOR) signaling pathways. Clenbuterol was administered to normal weight-bearing adult rats to examine the growth-inducing effects and to adult rats undergoing muscle atrophy as the result of hindlimb suspension or denervation to examine the muscle-sparing effects. The pharmacological inhibitor rapamycin was administered in combination with clenbuterol in vivo to determine whether activation of mTOR was involved in mediating the effects of clenbuterol. Clenbuterol administration increased the phosphorylation status of PKB/Akt, S6 kinase 1/p70s6k, and eukaryotic initiation factor 4E binding protein 1/PHAS-1. Clenbuterol treatment induced growth by 27–41% in normal rats and attenuated muscle loss during hindlimb suspension by 10–20%. Rapamycin treatment resulted in a 37–97% suppression of clenbuterol-induced growth and a 100% reduction of the muscle-sparing effect. In contrast, rapamycin was unable to block the muscle-sparing effects of clenbuterol after denervation. Clenbuterol was also shown to suppress the expression of the MuRF1 and MAFbx transcripts in muscles from normal, denervated, and hindlimb-suspended rats. These results demonstrate that the effects of clenbuterol are mediated, in part, through the activation of Akt and mTOR signaling pathways.
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Siedlecka, U., M. Arora, T. Kolettis, G. K. R. Soppa, J. Lee, M. A. Stagg, S. E. Harding, M. H. Yacoub, and C. M. N. Terracciano. "Effects of clenbuterol on contractility and Ca2+ homeostasis of isolated rat ventricular myocytes." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 5 (November 2008): H1917—H1926. http://dx.doi.org/10.1152/ajpheart.00258.2008.
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Clenbuterol, a compound classified as a β2-adrenoceptor (AR) agonist, has been employed in combination with left ventricular assist devices (LVADs) to treat patients with severe heart failure. Previous studies have shown that chronic administration of clenbuterol affects cardiac excitation-contraction coupling. However, the acute effects of clenbuterol and the signaling pathway involved remain undefined. We investigated the acute effects of clenbuterol on isolated ventricular myocyte sarcomere shortening, Ca2+ transients, and L-type Ca2+ current and compared these effects to two other clinically used β2-AR agonists: fenoterol and salbutamol. Clenbuterol (30 μM) produced a negative inotropic response, whereas fenoterol showed a positive inotropic response. Salbutamol had no significant effects. Clenbuterol reduced Ca2+ transient amplitude and L-type Ca2+ current. Selective β1-AR blockade did not affect the action of clenbuterol on sarcomere shortening but significantly reduced contractility in the presence of fenoterol and salbutamol ( P < 0.05). Incubation with 2 μg/ml pertussis toxin significantly reduced the negative inotropic effects of 30 μM clenbuterol. In addition, overexpression of inhibitory G protein (Gi) by adenoviral transfection induced a stronger clenbuterol-mediated negative inotropic effect, suggesting the involvement of the Gi protein. We conclude that clenbuterol does not increase and, at high concentrations, significantly depresses contractility of isolated ventricular myocytes, an effect not seen with fenoterol or salbutamol. In its negative inotropism, clenbuterol predominantly acts through Gi, and the consequent downstream signaling pathways activation may explain the beneficial effects observed during chronic administration of clenbuterol in patients treated with LVADs.
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He, Genye, Linghui Sheng, Jianli Zhang, Yun Wu, Xuxiao Zhao, Youxuan Xu, and Jianghai Lu. "Enantiomeric analysis of clenbuterol in Chinese people by LC–MS/MS to distinguish doping abuse from meat contamination." Bioanalysis 12, no. 11 (June 2020): 783–90. http://dx.doi.org/10.4155/bio-2020-0003.
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Aim: Follow-up investigations are often required for clenbuterol-positive cases. A method to distinguish doping abuse from meat contamination was developed. Materials & methods: A total of 26 volunteers were recruited to ingest clenbuterol contaminated-pork and clenbuterol tablets. Results: For 20 volunteers, after ingestion of contaminated-pork, R-(-)/S-(+)-clenbuterol ratio was <1.0, while the value was >1.0 after taking clenbuterol tablets. However, after taking clenbuterol tablets, some ratio points of the other six volunteers were between 0.9 and 1.0. A case of an abnormal cold and fever, which returned to normal after recovery, was also reported firstly. Conclusion: A change in R-(-)/S-(+)-clenbuterol was reported in the Chinese population initially. A ratio of 0.9 was recommended in doping related cases for the Chinese population.
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Luo, Ling, Peijing Hu, Changqing Miao, Aiqun Ma, and Tingzhong Wang. "Clenbuterol Attenuates hERG Channel by Promoting the Mature Channel Degradation." International Journal of Toxicology 36, no. 4 (May 24, 2017): 314–24. http://dx.doi.org/10.1177/1091581817710786.
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Clenbuterol, a β2-selective adrenergic receptor agonist, is illicitly used in weight loss and performance enhancement and animal production. Increasing evidence demonstrates that clenbuterol induces various kinds of arrhythmias and QTc interval prolongation. However, little is known about the underlying mechanism. Most drugs are associated with QTc prolongation through interfering with human ether-a-go-go-related gene (hERG) K+ channels. The present study aims to investigate the effects and underlying mechanisms of clenbuterol on the hERG channel. HEK 293 cells were transfected with wild type and Y652A or F656A mutants of the hERG channel and treated with clenbuterol. The hERG current was recorded using whole-cell patch-clamp technique, and protein level was evaluated by Western blot. We found that clenbuterol decreases the mature form of the hERG protein at the cell membrane in a concentration- and time-dependent manner, without affecting the immature form. Correspondingly, clenbuterol chronic treatment reduced hERG current to a greater extent compared to acute treatment. In the presence of Brefeldin A (BFA), which was used to block hERG channel trafficking to cell membrane, clenbuterol reduced hERG on plasma membrane to a greater extent than BFA alone. In addition, the hERG channel’s drug binding sites mutant Y652A and F656A abolished clenbuterol-mediated hERG reduction and current blockade. In conclusion, clenbuterol reduces hERG channel expression and current by promoting the channel degradation. The effect of clenbuterol on the hERG channel is related to the drug-binding sites, Tyr-652 and Phe-656, located on the S6 domain. This biophysical mechanism may underlie clenbuterol-induced QTc prolongation or arrhythmia.
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Van Der Heijden, H. F. M., P. N. R. Dekhuijzen, H. Folgering, L. A. Ginsel, and C. L. A. Van Herwaarden. "Long-term effects of clenbuterol on diaphragm morphology and contractile properties in emphysematous hamsters." Journal of Applied Physiology 85, no. 1 (July 1, 1998): 215–22. http://dx.doi.org/10.1152/jappl.1998.85.1.215.
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The aim of the present study was to investigate the effect of chronic long-term clenbuterol treatment (1 mg/kg subcutaneously twice a day for 12 wk) on diaphragm morphology and function in emphysematous (EH) and normal hamsters (NH). Clenbuterol increased body weight, diaphragm weight, and skeletal muscle weight in both EH and NH to a similar extent. In the diaphragm, clenbuterol significantly increased myosin heavy chain type I, IIa, and IIx muscle fiber cross-sectional areas by ∼35–55% in both EH and NH. This response to clenbuterol treatment was not significantly different between EH and NH diaphragm. In EH, twitch force (Pt), maximal tetanic force, and force-frequency curve were significantly reduced compared with NH. In EH, clenbuterol increased Pt by ∼10%, restoring Pt to NH level. A similar improvement was observed in the force-frequency characteristics. Clenbuterol did not alter contractile properties in NH. In conclusion, long-term clenbuterol treatment resulted in an increased size of all diaphragm muscle fiber types in both NH and EH. Clenbuterol completely abolished the reduced force generation induced by emphysema.
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Cavalié, H., G. Lac, P. Lebecque, B. Chanteranne, M. J. Davicco, and J. P. Barlet. "Influence of clenbuterol on bone metabolism in exercised or sedentary rats." Journal of Applied Physiology 93, no. 6 (December 1, 2002): 2034–37. http://dx.doi.org/10.1152/japplphysiol.00472.2002.
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This paper reports that the selective β2-adrenergic receptor agonist clenbuterol affects bone metabolism in growing 3-mo-old male Wistar rats treated over 8 wk. Thirty-two 3-mo-old growing Wistar rats weighing 234 ± 2 g were assigned to a progressive isometric force, strength-training exercise program plus oral clenbuterol (2 mg · kg body wt−1 · day−1) for 5 days each week, exercise program without clenbuterol 5 days each week, no exercise program plus oral clenbuterol (2 mg · kg−1 · day−1) for 5 days each week, or no exercise without clenbuterol 5 days each week. At the end of 8 wk, lean mass, fat mass, and right total femoral, distal metaphyseal femoral, and diaphyseal femoral bone mineral density were measured by Hologic QDR 4500 dual X-ray absorptiometry (DEXA) technique. Left femoral bones were harvested after death on day 58, and femoral resistance was determined by three-point bending testing. We found that fat mass was decreased in rats given strength training exercise and decreased further in rats treated with clenbuterol. Lean mass was increased in clenbuterol-treated animals. Strength-training exercise appeared to have no effect on bone mineral density, serum osteocalcin, or urinary deoxypyridinoline. However, clenbuterol treatment decreased femoral length, diameter, bone mineral density, and mechanical resistance. Clenbuterol had no effect on osteocalcin but increased urinary deoxypyridinoline. We concluded that clenbuterol treatment decreased bone mineral density and increased bone resorption independent of the level of exercise rats were given.
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Burniston, Jatin G., Yeelan Ng, William A. Clark, John Colyer, Lip-Bun Tan, and David F. Goldspink. "Myotoxic effects of clenbuterol in the rat heart and soleus muscle." Journal of Applied Physiology 93, no. 5 (November 1, 2002): 1824–32. http://dx.doi.org/10.1152/japplphysiol.00139.2002.
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Myocyte-specific necrosis in the heart and soleus muscle of adult male Wistar rats was investigated in response to a single subcutaneous injection of the anabolic β2-adrenergic receptor agonist clenbuterol. Necrosis was immunohistochemically detected by administration of a myosin antibody 1 h before the clenbuterol challenge and quantified by using image analysis. Clenbuterol-induced myocyte necrosis occurred against a background of zero damage in control muscles. In the heart, the clenbuterol-induced necrosis was not uniform, being more abundant in the left subendocardium and peaking 2.4 mm from the apex. After position (2.4 mm from the apex), dose (5 mg clenbuterol/kg), and sampling time (12 h) were optimized, maximum cardiomyocyte necrosis was found to be 1.0 ± 0.2%. In response to the same parameters (i.e., 5 mg of clenbuterol and sampled at 12 h), skeletal myocyte necrosis was 4.4 ± 0.8% in the soleus. These data show significant myocyte-specific necrosis in the heart and skeletal muscle of the rat. Such irreversible damage in the heart suggests that clenbuterol may be damaging to long-term health.
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Zhao, Xiangyun, Yuliang Mai, Dongchu Chen, Min Zhang, and Huawen Hu. "Selective Enrichment of Clenbuterol onto Molecularly Imprinted Polymer Microspheres with Tailor-made Structure and Oxygen Functionalities." Polymers 11, no. 10 (October 10, 2019): 1635. http://dx.doi.org/10.3390/polym11101635.
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The noxious clenbuterol misapplied as the feed additive has posed an enormous threat to humans who actively rely on the food chains with high potential of contamination by clenbuterol, such as pork and beef. It is, therefore, highly desirable to develop novel materials and strategies for dealing with the clenbuterol. Herein, functional polymer microspheres prepared by Pickering emulsion polymerization were explored for the selective enrichment of the clenbuterol, and their structure and oxygen functionalities could be tailor-made by a molecular imprinting process. The clenbuterol imprinting was adequately demonstrated to not only increase the particle size (~52 nm vs. ~42 nm) and create cavities for the accommodation of the clenbuterol molecules, but also reduce the oxygen functionalities of the resulting molecularly imprinted polymer microspheres (MIPMs) by approximately 4 at.%, which is believed to correlate with the high specificity of the MIPMs. Various characterization methods were employed to evidence these findings, including scanning electron microscopy, BET measurements, Fourier transform infrared spectroscopy, X-ray photoelectron spectroscopy, and elemental mapping examination. More importantly, the MIPMs showed a markedly superior enrichment capability towards clenbuterol to the counterpart, that is, non-molecularly imprinted polymer microspheres (NIPMs). Compared to the NIPMs without specificity for clenbuterol, the MIPMs exhibited an impressive selectivity to clenbuterol, with the relative selectivity coefficient (k′) values largely exceeding 1, thus corroborating that the useful molecular imprinting led to the generation of the binding sites complementary to the clenbuterol molecule in the size and functionalities. The MIPMs were also employed as the stationary phase to fabricate molecularly imprinting solid-phase extraction column, and the spike recovery was demonstrated to be not significantly decreased even after nine cycles. Furthermore, the reliability of the method was also evidenced through the comparison of the MIPMs prepared from different batches.
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Guo, Qinghui, Yankun Peng, Xinlong Zhao, and Yahui Chen. "Rapid Detection of Clenbuterol Residues in Pork Using Enhanced Raman Spectroscopy." Biosensors 12, no. 10 (October 11, 2022): 859. http://dx.doi.org/10.3390/bios12100859.
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Clenbuterol (CB) is a synthetic β-receptor agonist which can be used to improve carcass leanness in swine, but its residues in pork also pose health risks. In this report, surface-enhanced Raman scattering (SERS) technology was used to achieve rapid detection and identification of clenbuterol hydrochloride (CB) residues. First, the effects of several different organic solvents on the extraction efficiency were compared, and it was found that clenbuterol in pork had a better enhancement effect using ethyl acetate as an extraction agent. Then, SERS signals of clenbuterol in different solvents were compared, and it was found that clenbuterol had a better enhancement effect in an aqueous solution. Therefore, water was chosen as the solvent for clenbuterol detection. Next, enhancement effect was compared using different concentration of sodium chloride solution as the aggregating compound. Finally, pork samples with different clenbuterol content (1, 3, 5, 7, 9, and 10 µg/g) were prepared for quantitative analysis. The SERS spectra of samples were collected with 0.5 mol/L of NaCl solution as aggregating compound and gold colloid as an enhanced substrate. Multiple scattering correction (MSC) and automatic Whittaker filter (AWF) were used for preprocessing, and the fluorescence background contained in the original Raman spectra was removed. A unary linear regression model was established between SERS intensity at 1472 cm-1 and clenbuterol content in pork samples. The model had a better linear relationship with a correlation coefficient R2 of 0.99 and a root mean square error of 0.263 µg/g. This method can be used for rapid screening of pork containing clenbuterol in the market.
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Awede, Bonaventure L., Jean-Paul Thissen, and Jean Lebacq. "Role of IGF-I and IGFBPs in the changes of mass and phenotype induced in rat soleus muscle by clenbuterol." American Journal of Physiology-Endocrinology and Metabolism 282, no. 1 (January 1, 2002): E31—E37. http://dx.doi.org/10.1152/ajpendo.2002.282.1.e31.
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Clenbuterol induces hypertrophy and a slow-to-fast phenotype change in skeletal muscle, but the signaling mechanisms remain unclear. We hypothesized that clenbuterol could act via local expression of insulin-like growth factor I (IGF-I). Administration of clenbuterol to 3-mo-old female Wistar rats resulted in a 10 and 13% increase of soleus muscle mass after 3 and 9 days, respectively, reaching 16% after 4 wk. When associated with triiodothyronine, clenbuterol induced a dramatic slow-to-fast phenotype change. In parallel, clenbuterol administration induced in soleus muscle a fivefold increase in IGF-I mRNA levels associated with an eightfold increase in IGF-binding protein (IGFBP)-4 and a fivefold increase of IGFBP-5 mRNA levels on day 3. This increased IGF-I gene expression was associated with an increase in muscle IGF-I content, already detected on day 1 and persisting until day 5 without increase in serum IGF-I concentrations. These data show that muscle hypertrophy induced by clenbuterol is associated with a local increase in muscle IGF-I content. They suggest that clenbuterol-induced muscle hypertrophy could be mediated by local production of IGF-I.
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De Schrijver, R., D. Fremaut, and M. Van Den Broeck. "Effects of short-term feeding of clenbuterol on nitrogen retention, performance and meat quality in finishing pigs." Journal of Agricultural Science 116, no. 1 (February 1991): 105–9. http://dx.doi.org/10.1017/s002185960007619x.
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SUMMARYAn experiment using 30 Belgian landrace finishing pigs was carried out, in 1989, at the University of Leuven, Belgium, to examine the effect of clenbuterol in the diet (1 mg/kg) on the repartitioning of nutrients and body composition. Clenbuterol was administered for 20 days preceding the week before slaughter. Fifteen animals were fed a diet containing the β-agonist, and 15 other animals served as negative controls. Weight gain, feed conversion and N utilization improved during β-agonist treatment. Removal of clenbuterol from the diet rapidly increased blood urea concentrations, indicating immediate, less efficient, N utilization. In the week before slaughter, the animals did not lose the extra weight gained in the period of clenbuterol feeding. Backfat thickness at slaughter was reduced by 15% in the animals fed clenbuterol. Dressing percentage and post mortem pH decline, colour and water-holding capacity in ham and the longissimus dorsi were not affected by dietary treatment. Clenbuterol was not detected in renal fat and the longissimus dorsi at slaughter.
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Oblak, Marko, Andrej Preželj, Slavko Pečar, and Tom Solmajer. "Thiol-reactive Clenbuterol Analogues Conjugated to Bovine Serum Albumin." Zeitschrift für Naturforschung C 59, no. 11-12 (December 1, 2004): 880–86. http://dx.doi.org/10.1515/znc-2004-11-1219.
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Several novel thiol-reactive clenbuterol analogues were coupled in high yield with bovine serum albumin (BSA). After labelling of unreacted cysteines with maleimide spin label (MiSL), the yield of the coupling reaction was determined by electron paramagnetic resonance (EPR) spectroscopy and spectral analysis. Two spin-probe populations with different mobility states were quantitatively determined. Molecular dynamics was used to model the structure of clenbuterol analogues and spin label conjugated to BSA and recognition of conjugates by anti-clenbuterol antibodies was demonstrated. The recognition of BSA-A, BSA-C and BSAS conjugates with monoclonal and polyclonal anti-clenbuterol (mCLB-Ab and rCLB-Ab) antibodies was an indication, that chlorine substituents on the aromatic ring of clenbuterol derivatives are not necessary for the binding of antibodies to the conjugates. These results confirmed the importance of the tert-butylamino group as a part of the epitope and contribute to the understanding of the recognition process with anti-clenbuterol antibodies.
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Ricart-Firinga, Carole, Laurence Stevens, Marie-Helene Canu, Tatiana L. Nemirovskaya, and Yvonne Mounier. "Effects of β2-agonist clenbuterol on biochemical and contractile properties of unloaded soleus fibers of rat." American Journal of Physiology-Cell Physiology 278, no. 3 (March 1, 2000): C582—C588. http://dx.doi.org/10.1152/ajpcell.2000.278.3.c582.
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The effects of clenbuterol β2-agonist administration were investigated in normal and atrophied [15-day hindlimb-unloaded (HU)] rat soleus muscles. We showed that clenbuterol had a specific effect on muscle tissue, since it reduces soleus atrophy induced by HU. The study of Ca2+ activation properties of single skinned fibers revealed that clenbuterol partly prevented the decrease in maximal tension after HU, with a preferential effect on fast-twitch fibers. Clenbuterol improved the Ca2+ sensitivity in slow- and fast-twitch fibers by shifting the tension-pCa relationship toward lower Ca2+ concentrations, but this effect was more marked after HU than in normal conditions. Whole muscle electrophoresis indicated slow-to-fast transitions of the myosin heavy chain isoforms for unloaded and for clenbuterol-treated soleus. The coupling of the two latter conditions did not, however, increase these phenotypical transformations. Our findings indicated that clenbuterol had an anabolic action and a β2-adrenergic effect on muscle fibers and appeared to counteract some effects of unloading disuse conditions.
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&NA;. "Clenbuterol abuse." Reactions Weekly &NA;, no. 1167 (September 2007): 11. http://dx.doi.org/10.2165/00128415-200711670-00031.
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&NA;. "Clenbuterol abuse." Reactions Weekly &NA;, no. 1246 (April 2009): 13. http://dx.doi.org/10.2165/00128415-200912460-00032.
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Ishikawa, Chieko, Takumi Ogawa, Tomoko Ikawa, and Akira Yamane. "Effects of Clenbuterol, a β2-Adrenergic Agonist, on Sizes of Masseter, Temporalis, Digastric, and Tongue muscles." Open Dentistry Journal 3, no. 1 (September 7, 2009): 191–96. http://dx.doi.org/10.2174/1874210600903010191.
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We compared the hypertrophic effects of clenbuterol, a β2-adrenergic agonist, on the masseter, digastric, and temporalis with those on the tongue, tibialis anterior, soleus, diaphragm, and heart. The weights of masseter, digastric and temporalis in the clenbuterol group were 36 ~ 56% greater than those in the control group, whereas those of the tibialis anterior, diaphragm, and heart weights in the clenbuterol group were 9 ~ 33% greater than those in the control group. No significant difference in the weights of the soleus and tongue was found between the control and clenbuterol groups. Taken together with our present and previously reported results, it is suggested that the hypertrophic effects of clenbuterol on the masseter, digastric, and temporalis are greater than those on the limb, trunk, and heart.
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Moore, D., M. Anderson, and DF Larson. "Effect of clenbuterol administration on the healthy murine heart." Perfusion 23, no. 5 (September 2008): 297–302. http://dx.doi.org/10.1177/0267659109104688.
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Clenbuterol has recently been shown to reverse pathologic cardiac remodeling during left ventricular assist device (LVAD) support, leading to restored ventricular function and explantation of LVAD devices. However, others have not been able to support these observations. Our hypothesis is that the β2-adrenergic activity of clenbuterol induces cardiac extracellular matrix (ECM) remodeling, resulting in increased interstitial fibrillar collagen content and altered diastolic function that may account for these conflicting reports. The intent of this study is to characterize the effect of clenbuterol on healthy murine hearts with transthoracic echo and histology. C57BL/6 female mice were administered 2.4 µg/kg/day of clenbuterol in the drinking water for 7 days and analysis conducted on day 8–24 hours after the last dose of clenbuterol. Histological analysis demonstrated an increase in left ventricular ECM collagen content in a control group compared with the clenbuterol group (density 0.32 ± 0.16 compared to 2.01 ± 0.30 RD/mm2). The ventricular fibrosis was supported by altered diastolic function measured by transthoracic echo where there was a significant increase in isovolumic relaxation time, and left atrial dimension and a decrease in left ventricular free wall tissue Doppler ratios. Our study showed no significant differences in left ventricular ejection fraction, cardiac output, or heart rate between the clenbuterol and control groups. These data suggest that the β-2 adrenergic activity of clenbuterol increases ECM fibrillar collagen concentrations in normal hearts, resulting in altered diastolic function.
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Torgan, C. E., G. J. Etgen, J. T. Brozinick, R. E. Wilcox, and J. L. Ivy. "Interaction of aerobic exercise training and clenbuterol: effects on insulin-resistant muscle." Journal of Applied Physiology 75, no. 4 (October 1, 1993): 1471–76. http://dx.doi.org/10.1152/jappl.1993.75.4.1471.
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The effects of aerobic exercise training, chronic administration of the selective beta 2-adrenergic agonist clenbuterol, and the combination of these two treatments on muscle insulin resistance were compared in female obese (fa/fa) Zucker rats. Rats were randomly assigned to trained, clenbuterol, clenbuterol-trained, or control groups. Training consisted of treadmill running for 2 h/day at 18 m/min up an 8% grade. Clenbuterol was administered by intubation (0.4–0.8 mg.kg body wt-1 x day-1) approximately 30 min before the rats ran each day. After 8 wk of treatment, muscle insulin resistance was assessed via hindlimb perfusion in the presence of 8 mM glucose and a submaximal (500 microU/ml) insulin concentration. Training increased citrate synthase activity (mumol.g wet wt-1 x min-1) by 32–74% and insulin-stimulated glucose uptake by 45%. Clenbuterol ingestion induced a 17–29% increase in muscle mass but decreased citrate synthase activity by 34–42% and had no effect on muscle glucose uptake. Administration of clenbuterol to rats that exercise trained prevented the training-induced improvement in insulin-stimulated glucose uptake and attenuated the increases in citrate synthase activity. In addition, both clenbuterol-treated groups displayed a 42% decrease in beta-adrenergic receptor density. The results indicate that clenbuterol administration, possibly through beta-adrenergic receptor downregulation, attenuated a cellular reaction essential for the exercise training-induced increase in citrate synthase activity and improvement in skeletal muscle insulin resistance of the obese Zucker rat.
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Williams, P. E. V., L. Pagliani, G. M. Innes, K. Pennie, C. I. Harris, and P. Garthwaite. "Effects of a β-agonist (clenbuterol) on growth, carcass composition, protein and energy metabolism of veal calves." British Journal of Nutrition 57, no. 3 (May 1987): 417–28. http://dx.doi.org/10.1079/bjn19870049.
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1. Twenty-two British Friesian bull calves were used in a comparative slaughter experiment to determine the effects of a β-agonist (clenbuterol) on body composition and energy retention. Four calves were slaughtered at 18 d of age and constituted the initial slaughter group. Of the remaining calves, eight (group A, controls) were given milk replacer only, and ten calves (groups B and C, five calves per group) were given milk replacer plus clenbuterol(O.1 and 1.0 mg clenbuterol/kg milk replacer equivalent to approximately 2 and 20 μg/kg body-weight respectively over the 105±3 d of the experimental period). Calves were slaughtered over the weight range 146–177 kg.2. Clenbuterol had no significant effect on dry matter (DM) intake, daily live-weight gain or feed conversion ratio. DM digestibility of the milk replacer was not affected by treatment. Nitrogen balance was measured on three separate occasions starting when the calves weighed approximately 60, 110 and 130 kg. N retention was increased over the experimental period in clenbuterol-treated calves, although the effect only achieved significance in calves weighing approximately 110 kg live weight (P < 0.05).3. Clenbuterol (20 μg/kg body-weight) increased estimated mean daily N retention in the carcass of the calves from 22 to 25 g whilst N retention in the non-carcass components decreased from 10 to 8 g/d. Effects of clenbuterol on N retention occurred mainly in skeletal muscle. Fat in both carcass and non-carcass components was reduced by treatment with clenbuterol. The total energy content of live-weight gain was reduced from 1077 to 897 MJ in clenbuterol-treated calves and mean daily heat production was estimated to increase from 23.1 in controls to 25.9 MJ/d in calves in group C.4. In calves of mean live weight during balance of 120 and 136 kg, clenbuterol significantly increased daily urinary creatinine excretion and in 120 kg calves NT-methylhistidine was significantly decreased (P < 0.05). Based on estimates of muscle mass from urinary creatinine and protein degradation fromN7-methylhistidine NT-methylhistidine excretion, the fractional breakdown rate of muscle protein in clenbuterol-treated calves was only 0.66 of that in the controls when the calves weighed 120 kg.
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Velasco-Bejarano, Benjamín, Jahir Bautista, Martha E. Rodríguez, Raquel López-Arellano, Roberto Arreguín-Espinosa, and Ricardo Velasco Carrillo. "Quantification and Stereochemical Composition of R-(−) and S-(+)-Clenbuterol Enantiomers in Bovine Urine by Liquid Chromatography–Tandem Mass Spectrometry." Journal of Analytical Toxicology 44, no. 3 (November 4, 2019): 237–44. http://dx.doi.org/10.1093/jat/bkz087.
Full textAbstract:
Abstract Clenbuterol (4-amino-α-[(tert-butylamino)methyl]-3,5-dichlorobenzylalcohol) is a β2-adrenergic agonist. The consumption of meat contaminated with clenbuterol can lead to increased heart rate, blood pressure, anxiety, palpitations and skeletal muscle tremors. Several analytical methods have been developed to identify and quantify clenbuterol in different biological matrices. In this report, we have developed a specific and sensitive analytical method for quantifying clenbuterol and performed an in-depth enantiomeric analysis in bovine urine. The method was evaluated in accordance with international guidelines, and we used an isotopically labeled analog as an internal standard. The extraction efficiency for clenbuterol in bovine urine was > 98%, the limit of detection was 0.05 ng/mL and the limit of quantification was 0.10 ng/mL. Our assay showed high specificity, no carryover was observed and the assay was linear in the range 0.10–8.0 ng/mL. Fifteen bovine urine samples were analyzed (containing clenbuterol), and an enantiomeric analysis was performed. The clenbuterol concentration range was 0.10–10.56 ng/mL across these samples. The levorotatory enantiomer was detected at greater concentrations than the dextrorotatory enantiomer, the ratio being 1.7 ± 0.6 (n = 15), and a statistical difference was observed (P < 0.05) using the Wilcoxon test.
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Dupont-Versteegden, E. E. "Exercise and clenbuterol as strategies to decrease the progression of muscular dystrophy in mdx mice." Journal of Applied Physiology 80, no. 3 (March 1, 1996): 734–41. http://dx.doi.org/10.1152/jappl.1996.80.3.734.
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The effects of exercise and the combination of exercise and clenbuterol on progression of muscular dystrophy were studied in mdx mice. At 3 wk of age, mdx mice were randomly assigned to sedentary (MS), exercise (ME), or combined exercise and clenbuterol (MEC) groups. Clenbuterol was given in the drinking water (1.0-1.5 mg . kg body weight-1 . day-1), and exercise consisted of spontaneous running activity on exercise wheels. At 3 mo or 1 yr of age, ventilatory function, contractile properties, and morphological characteristics of the soleus (Sol) and diaphragm (Dia) muscles were measured. The mdx mice receiving clenbuterol ran less than the mice without clenbuterol. The combination of clenbuterol and exercise was associated with an increase in Sol muscle weight and a muscle weight-to-body weight ratio of 30-35% compared with the sedentary group and approximately 20% compared to exercise alone. Myosin and total protein concentrations of the Sol and Dia increased in the MEC group at 1 yr of age only. Normalized active tension was increased in the Dia at 1 yr of age in both the ME and MEC groups by approximately 30%. Absolute tetanic tension of the Sol was increased at both 3 mo and 1 yr of age in the MEC compared with the MS group. At 1 yr of age, there was an additional 23% increase compared with the ME group. Fatigability increased in the MEC group by approximately 25% in the Sol and Dia muscles at both ages compared with the MS and ME groups. Results indicate that exercise and exercise plus clenbuterol decrease the progression of muscular dystrophy. However, different mechanisms may be involved because the combination of clenbuterol and exercise resulted in increased fatigability and the development of deformities, whereas exercise alone did not. Therefore, clenbuterol may not be suitable for use in patients with muscular dystrophy.
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Ryall, James G., Paul Gregorevic, David R. Plant, Martin N. Sillence, and Gordon S. Lynch. "β2-Agonist fenoterol has greater effects on contractile function of rat skeletal muscles than clenbuterol." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 6 (December 1, 2002): R1386—R1394. http://dx.doi.org/10.1152/ajpregu.00324.2002.
Full textAbstract:
Potential treatments for skeletal muscle wasting and weakness ideally possess both anabolic and ergogenic properties. Although the β2-adrenoceptor agonist clenbuterol has well-characterized effects on skeletal muscle, less is known about the therapeutic potential of the related β2-adrenoceptor agonist fenoterol. We administered an equimolar dose of either clenbuterol or fenoterol to rats for 4 wk to compare their effects on skeletal muscle and tested the hypothesis that fenoterol would produce more powerful anabolic and ergogenic effects. Clenbuterol treatment increased fiber cross-sectional area (CSA) by 6% and maximal isometric force (Po) by 20% in extensor digitorum longus (EDL) muscles, whereas fiber CSA in soleus muscles decreased by 3% and Po was unchanged, compared with untreated controls. In the EDL muscles, fenoterol treatment increased fiber CSA by 20% and increased Po by 12% above values achieved after clenbuterol treatment. Soleus muscles of fenoterol-treated rats exhibited a 13% increase in fiber CSA and a 17% increase in Po above that of clenbuterol-treated rats. These data indicate that fenoterol has greater effects on the functional properties of rat skeletal muscles than clenbuterol.
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Hayes, Alan, and David A. Williams. "Contractile properties of clenbuterol-treatedmdx muscle are enhanced by low-intensity swimming." Journal of Applied Physiology 82, no. 2 (February 1, 1997): 435–39. http://dx.doi.org/10.1152/jappl.1997.82.2.435.
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Hayes, Alan, and David A. Williams. Contractile properties of clenbuterol-treated mdxmuscle are enhanced by low-intensity swimming. J. Appl. Physiol. 82(2): 435–439, 1997.—The β2-agonist clenbuterol has potent anabolic properties in normal and denervated muscle and, as such, may be of use in muscle wasting diseases such as muscular dystrophy. However, potential side effects such as the transformation of the fiber type pool toward increased proportions of fast-twitch fibers must be balanced with the beneficial anabolic properties. In the present report, we clearly show that extensor digitorum longus and soleus muscles from dystrophic mdxmice exposed to a combination of clenbuterol and low-intensity endurance swimming exercise did not undergo the slow- to fast-twitch fiber transformations caused by clenbuterol administration alone, yet increases in the force-generating capacity of the soleus (30–40%) that resulted from the clenbuterol treatment were maintained after the swimming program. The increased sensitivity of dystrophin-deficient dystrophic muscle to clenbuterol and low-intensity exercise that is evident in this study may have therapeutic implications in the treatment of muscle wasting diseases.
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Bakker, Anthony J., Stewart I. Head, Anthony C. Wareham, and D. George Stephenson. "Effect of clenbuterol on sarcoplasmic reticulum function in single skinned mammalian skeletal muscle fibers." American Journal of Physiology-Cell Physiology 274, no. 6 (June 1, 1998): C1718—C1726. http://dx.doi.org/10.1152/ajpcell.1998.274.6.c1718.
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We examined the effect of the β2-agonist clenbuterol (50 μM) on depolarization-induced force responses and sarcoplasmic reticulum (SR) function in muscle fibers of the rat ( Rattus norvegicus; killed by halothane overdose) that had been mechanically skinned, rendering the β2-agonist pathway inoperable. Clenbuterol decreased the peak of depolarization-induced force responses in the extensor digitorum longus (EDL) and soleus fibers to 77.2 ± 9.0 and 55.6 ± 5.4%, respectively, of controls. The soleus fibers did not recover. Clenbuterol significantly and reversibly reduced SR Ca2+loading in EDL and soleus fibers to 81.5 ± 2.8 and 78.7 ± 4.0%, respectively, of controls. Clenbuterol also produced an ∼25% increase in passive leak of Ca2+ from the SR of the EDL and soleus fibers. These results indicate that clenbuterol has direct effects on fast- and slow-twitch skeletal muscle, in the absence of the β2-agonist pathway. The increased Ca2+ leak in the triad region may lead to excitation-contraction coupling damage in the soleus fibers and could also contribute to the anabolic effect of clenbuterol in vivo.
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Maltin, C. A., M. I. Delday, S. M. Hay, F. G. Smith, and P. J. Reeds. "Propranolol apparently separates the physical and compositional characteristics of muscle growth induced by clenbuterol." Bioscience Reports 7, no. 1 (January 1, 1987): 51–57. http://dx.doi.org/10.1007/bf01122727.
Full textAbstract:
The effect of propranolol on clenbuterol-induced changes in muscle fibre size and protein content were studied. Propranolol did not inhibit the ability of clenbuterol to stimulate protein accretion but reduced the increase in muscle fibre size. The compositional and physical characteristics of clenbuterol-induced muscle growth thus appeared to be separated by propranolol.
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Drake, S. D., L. E. Hansen, C. Harris, W. C. Lewis, E. Miller, B. Moranville, M. Blyzka, et al. "Effects of clenbuterol on horses." Comparative Exercise Physiology 9, no. 3-4 (January 1, 2013): 181–87. http://dx.doi.org/10.3920/cep13022.
Full textAbstract:
Clenbuterol was intended as a treatment for respiratory diseases in horses, but has been used in multiple species, including humans, for its repartitioning of fat to lean effects (free fatty acids are released from adipose tissue to be used by tissues of higher priority). In the horse industry clenbuterol application is restricted to the treatment of chronic obstructive pulmonary disease and reactive airway disease (heaves). Negative effects of clenbuterol exposure include a decrease in maximum oxygen intake and increased muscle fatigue upon exercise. As a result of these and other negative effects, clenbuterol remains strictly controlled by the US Food and Drug Administration.
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McElligott, M. A., J. E. Mulder, L. Y. Chaung, and A. Barreto. "Clenbuterol-induced muscle growth: investigation of possible mediation by insulin." American Journal of Physiology-Endocrinology and Metabolism 253, no. 4 (October 1, 1987): E370—E375. http://dx.doi.org/10.1152/ajpendo.1987.253.4.e370.
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The role of insulin as a possible mediator of the beta-adrenergic agonist stimulation of muscle growth was investigated. To exclude possible action of the beta-agonist on the pancreatic release of insulin, diabetes was induced in rats by a streptozotocin injection (100 mg/kg). Insulin levels were almost not detectable in these rats. Feeding either normal diet or diet containing the beta-adrenergic agonist clenbuterol (10 parts/million) did not alter plasma insulin concentrations. The effects of clenbuterol on muscle and weight gain were determined in diabetic rats given daily insulin replacement (D + I) and fed either a normal diet or clenbuterol-treated diet. Clenbuterol, fed for 1 wk, increased the wet weight of the gastrocnemius, soleus, and extensor digitorum longus muscles (15-23%) in both normal and D + I rats. Although clenbuterol increased body weight gain, it did not alter feed consumption and, therefore, feed efficiency (g gain/g food) was improved. Activities of cathepsin B and N-acetyl-beta-glucosaminidase, but not cathepsin D, were elevated in the soleus muscles of clenbuterol-treated rats. The clenbuterol-induced increase in muscle growth in the insulin-replaced diabetic rats indicated that this beta-adrenergic agonist effect was not mediated by an alteration of circulating levels of insulin, secondary to beta-agonist action on pancreatic insulin release.
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Zhu, Yuan, Carsten Culmsee, Irina Semkova, and Josef Krieglstein. "Stimulation of β2-Adrenoceptors Inhibits Apoptosis in Rat Brain after Transient Forebrain Ischemia." Journal of Cerebral Blood Flow & Metabolism 18, no. 9 (September 1998): 1032–39. http://dx.doi.org/10.1097/00004647-199809000-00013.
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We have previously demonstrated that the neuroprotective effect of the β2-adrenoceptor agonist clenbuterol in vitro and in vivo was most likely mediated by an increased nerve growth factor (NGF) expression. In the present study, we examined whether clenbuterol was capable of inhibiting apoptosis caused by ischemia. Transient forebrain ischemia was performed in male Wistar rats (300 to 350 g) by clamping both common carotid arteries and reducing the blood pressure to 40 mm Hg for 10 minutes. Clenbuterol(0.1, 0.5, and 1.0 mg/kg intraperitoneally) was administered 3 hours before ischemia or immediately after ischemia. The brains were removed for histologic evaluation 7 days after ischemia. The time course of DNA fragmentation was determined 1, 2, 3 and 4 days after ischemia. Staining with terminal deoxynucleotidyl transferase(TdT)-mediated dUTP nick end-labeling (TUNEL) was used for further analysis of DNA fragments in situ 3 days after ischemia. The NGF protein was assayed by enzyme-linked immunosorbent assay. Ten-minute forebrain ischemia damaged 80% to 90% of the neurons in the hippocampal CA1 region evaluated 7 days after ischemia. Pretreatment with clenbuterol (0.5 and 1.0 mg/kg) reduced the neuronal damage by 18.1% ( P< 0.01) and 13.1% ( P < 0.05), respectively. The neuroprotective effect also was found when clenbuterol (0.5 mg/kg) was administered immediately after ischemia ( P < 0.05). The DNA laddering appeared in striatum 1 day and in hippocampus 2 days after ischemia and peaked on the third day in both regions. The DNA laddering was nearly abolished in the hippocampus and partially blocked in striatum and cortex by 0.5 mg/kg clenbuterol. These results were confirmed by TUNEL staining. Clenbuterol (0.5 mg/kg intraperitoneally) elevated the NGF protein level by 33% ( P < 0.05) in the hippocampus and 41% ( P < 0.05) in the cortex 6 hours after ischemia. Three days after ischemia, the NGF levels in these regions were no longer different between the clenbuterol-treated and control groups. This study clearly demonstrates that clenbuterol possesses a neuroprotective activity and a marked capacity to inhibit DNA degradation after global ischemia. The results suggest that clenbuterol increases NGF expression during the first hours after global ischemia and thereby protects neurons against apoptotic damage.
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Bates, P. C., and J. M. Pell. "Action and interaction of growth hormone and the β-agonist, clenbuterol, on growth, body composition and protein turnover in dwarf mice." British Journal of Nutrition 65, no. 2 (March 1991): 115–29. http://dx.doi.org/10.1079/bjn19910074.
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The responses of dwarf mice to dietary administration of clenbuterol (3 mg/kg diet), daily injections of growth hormone (15 μg/mouse per d) or both treatments combined were investigated and their actions, and any interactions, on whole-body growth, composition and protein metabolism, and muscle, liver and heart growth and protein metabolism, were studied at days 0, 4 and 8 of treatment. Growth hormone, with or without clenbuterol, induced an increase in body-weight growth and tail length growth; clenbuterol alone did not affect body-weight or tail length. Both growth hormone and clenbuterol reduced the percentage of whole-body fat and increased the protein:fat ratio. They also increased protein synthesis rates of whole body and muscle, although the magnitude of the increase was greater in response to growth hormone than to clenbuterol. Clenbuterol specifically induced growth of muscle, with a decrease in liver protein content, whereas growth hormone exhibited more general anabolic effects on tissue protein. Previous reports have suggested that effects of clenbuterol on skeletal muscle are mediated, at least in part, via decreased rates of protein degradation; we could find little evidence of any decrease in whole-body or tissue protein degradation and anabolic effects were largely due to increases in protein synthesis rates. However, small increases in muscle protein degradation rate were observed in response to growth hormone. Growth hormone induced a progressive increase in serum insulin-like growth factor-1 concentration, whereas there was no change with clenbuterol administration. Anabolic effects on whole-body and skeletal muscle protein metabolism, therefore, appear to be initially via independent mechanisms but are finally mediated by a common response (increased protein synthesis) in dwarf mice.
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Choo, J. J., M. A. Horan, R. A. Little, and N. J. Rothwell. "Anabolic effects of clenbuterol on skeletal muscle are mediated by beta 2-adrenoceptor activation." American Journal of Physiology-Endocrinology and Metabolism 263, no. 1 (July 1, 1992): E50—E56. http://dx.doi.org/10.1152/ajpendo.1992.263.1.e50.
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The potent anabolic effects of the beta 2-adrenoceptor agonist clenbuterol on skeletal muscle have been reported to be independent of actions on beta-adrenoceptors. In the present study clenbuterol, presented to rats in the diet (4 mg/kg), caused significant increases in gastrocnemius muscle mass, protein, and RNA content and a decrease in epididymal fat pad mass. These effects were not mimicked by oral administration of the beta 2-adrenoceptor agonist salbutamol even at high dose (52 mg/kg diet), and the effects of clenbuterol were not inhibited by addition of DL-propranolol (200 mg/kg diet). However, the selective beta 2-antagonist ICI-118,551 (200 mg/kg diet) reversed the anabolic effects of clenbuterol, and a high dose of DL-propranolol (1,000 mg/kg diet) also inhibited these actions of clenbuterol. Furthermore, continuous infusion of salbutamol (1.15 mg.kg body wt-1.day-1) via miniosmotic pumps did cause significant increases in muscle mass, protein, and RNA content. These results indicate that the anabolic effects of clenbuterol are dependent on interaction with the beta 2-adrenoceptor. However, a long duration of action appears to be required to induce the anabolic effects of beta 2-agonists.
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Babij, P., and F. W. Booth. "Clenbuterol prevents or inhibits loss of specific mRNAs in atrophying rat skeletal muscle." American Journal of Physiology-Cell Physiology 254, no. 5 (May 1, 1988): C657—C660. http://dx.doi.org/10.1152/ajpcell.1988.254.5.c657.
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It is known that denervation or hindlimb suspension both decrease the content of rRNA, alpha-actin mRNA, and cytochrome c mRNA in adult rat skeletal muscle. In the present study, the provision of clenbuterol (an anabolic agent) to adult female rats during a 7-day period of denervation of the soleus and gastrocnemius muscles prevented entirely the loss of rRNA, alpha-actin mRNA, and cytochrome c mRNA that normally occurs in denervated muscle. Although clenbuterol inhibited most of the loss of alpha-actin mRNA that occurred in the soleus and gastrocnemius muscles after 7 days of hindlimb suspension, clenbuterol administration had less effect on preventing the loss of rRNA and cytochrome c mRNA in hindlimb suspended skeletal muscle. Clenbuterol had no effect on protein content in atrophied muscle resulting from denervation or suspension. These data suggest that clenbuterol can maintain the expression of certain RNAs in atrophying adult rat skeletal muscle.
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Gibbs, Rachel L., Rebecca M. Swanson, Joslyn K. Beard, Ty B. Schmidt, Jessica L. Petersen, and Dustin T. Yates. "258 Deficits in growth, muscle mass, and body composition following intrauterine growth restriction persisted in lambs at 60 d of age but were improved by daily clenbuterol supplementation." Journal of Animal Science 98, Supplement_4 (November 3, 2020): 199. http://dx.doi.org/10.1093/jas/skaa278.367.
Full textAbstract:
Abstract Intrauterine growth restriction (IUGR) reduces neonatal muscle growth and alters body composition in livestock. Our objective was to determine the effect of IUGR on juvenile growth and assess the benefits of treatment with clenbuterol (β2 adrenergic agonist) in IUGR offspring. Heat stress-induced IUGR lambs were born 28% lighter (P < 0.05) than controls. At 60 d of age, unsupplemented IUGR lambs had reduced (P < 0.05) bodyweight (BW), average daily gain, and crown-rump length compared to controls, but clenbuterol-supplemented IUGR lambs did not differ from controls. Crown circumference, body girth, and cannon bone length did not differ among groups. Bioelectrical impedance in live lambs and carcasses estimated that lean mass and mass of multiple muscle groups were reduced (P < 0.05) in unsupplemented IUGR lambs but not clenbuterol-supplemented IUGR lambs compared to controls. Estimated protein, fat, and protein/fat were likewise reduced (P < 0.05) in unsupplemented but not clenbuterol-supplemented IUGR lambs. Loin-eye area in chilled carcasses was 30% smaller (P < 0.05) in unsupplemented IUGR lambs but 19% larger (P < 0.05) in clenbuterol-supplemented IUGR lambs compared to controls. Proximate analysis revealed greater (P < 0.05) fat and reduced (P < 0.05) protein and protein/fat in loin muscles from unsupplemented but not clenbuterol-supplemented IUGR lambs compared to controls. At necropsy, hindlimbs, hearts, and flexor digitorum superficialis muscles tended to be lighter (P ≤ 0.09) and lungs and kidneys were lighter (P < 0.05) in IUGR lambs. Kidney weight was further reduced (P < 0.05) in clenbuterol-supplemented IUGR lambs. Brain/BW tended to be reduced (P ≤ 0.09) and lung/BW and kidney/BW were reduced (P < 0.05) in IUGR lambs, but lung weight and lung/BW were greater (P < 0.05) in clenbuterol-supplemented compared to unsupplemented IUGR lambs. We conclude that poor growth and asymmetric body composition previously observed in IUGR neonates persists in juveniles, but daily treatment with clenbuterol recovered growth and improved body composition in IUGR lambs.
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Sillence, M. N., M. L. Matthews, T. W. Badran, and G. G. Pegg. "Effects of clenbuterol on growth in underfed cattle." Australian Journal of Agricultural Research 51, no. 3 (2000): 401. http://dx.doi.org/10.1071/ar99109.
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This study examined the effects of clenbuterol on the growth of young cattle (160 kg) that were fed a restricted quantity of a low-quality hay to simulate dry-season pasture conditions in the tropics. Twenty Brahman steers were used. Ten control animals lost an average of 0.24 kg/day in the first 17 days, then maintained their liveweight for the remaining 21 days of the experiment. By contrast, 10 clenbuterol-treated animals lost 0.3 kg/day for the first 17 days of the experiment, then continued to lose weight at a steady rate of 0.15 kg/day. In control steers, plasma concentrations of urea-nitrogen decreased over the course of the experiment, and this effect was accelerated by clenbuterol treatment (P < 0.05). There were no marked changes in plasma concentrations of glucose, potassium, or Nt-methylhistidine in response to clenbuterol treatment. Clenbuterol had no effect on β2 -adrenoceptor density in the longissimus muscle, but there was a marked increase in β2-adrenoceptors in both groups of cattle over time. Despite their loss of liveweight, the carcasses of clenbuterol-treated cattle were not lighter than controls (74.3 v. 72 kg, respectively) and contained 10% more protein (P < 0.05). This was reflected by a trend towards increased weight of the biceps femoris muscle (9%; P < 0.1). These findings are consistent with clenbuterol causing a drive to deposit muscle protein at the expense of other tissues, even when dietary protein and energy are limited.
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MacLennan, P. A., and R. H. Edwards. "Effects of clenbuterol and propranolol on muscle mass. Evidence that clenbuterol stimulates muscle β-adrenoceptors to induce hypertrophy." Biochemical Journal 264, no. 2 (December 1, 1989): 573–79. http://dx.doi.org/10.1042/bj2640573.
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1. A single subcutaneous injection of clenbuterol hydrochloride (0.125 mg/kg body wt.) to female Wistar rats produced a rapid increase in muscle cyclic AMP and lactate concentrations and a decrease in muscle glycogen concentrations. These changes are characteristic of muscle beta-adrenoceptor stimulation and were abolished by intraperitoneal injection of propranolol (12.5 mg/kg) 15 min before clenbuterol administration. 2. When this dose of clenbuterol was injected twice daily, the changes in muscle metabolite concentrations which followed its acute administration persisted until day 7 of treatment, and were accompanied by increases in muscle mass, body weight and muscle protein synthesis rate (ks). When the clenbuterol injections were preceded by propranolol injections (12.5 mg/kg administered according to the protocol described above), or if animals were treated with propranolol only, the values of these variables were not significantly different from those of sham-injected controls. 3. In rats fed on a semi-synthetic diet (PW3) supplemented with 2 mg of clenbuterol/kg of diet for 7 days, the muscle mass was greater than that of rats fed on unsupplemented PW3. The increased muscle mass was accompanied by increased muscle lactate and decreased muscle glycogen concentrations. When PW3 was supplemented with 2 mg of clenbuterol/kg and 200 mg of propranolol/kg, the increase in muscle mass remained, but decreased muscle glycogen concentrations and increased muscle lactate concentrations were also observed. 4. These data are consistent with the hypothesis that clenbuterol influences muscle growth via beta-adrenoceptor stimulation.
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Pan, Shujia J., Joe Hancock, Zhenping Ding, Donovan Fogt, Mancheong Lee, and John L. Ivy. "Effects of clenbuterol on insulin resistance in conscious obese Zucker rats." American Journal of Physiology-Endocrinology and Metabolism 280, no. 4 (April 1, 2001): E554—E561. http://dx.doi.org/10.1152/ajpendo.2001.280.4.e554.
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The present study was conducted to determine the effect of chronic administration of the long-acting β2-adrenergic agonist clenbuterol on rats that are genetically prone to insulin resistance and impaired glucose tolerance. Obese Zucker rats ( fa/fa) were given 1 mg/kg of clenbuterol by oral intubation daily for 5 wk. Controls received an equivalent volume of water according to the same schedule. At the end of the treatment, rats were catheterized for euglycemic-hyperinsulinemic (15 mU insulin · kg−1 · min−1) clamping. Clenbuterol did not change body weight compared with the control group but caused a redistribution of body weight: leg muscle weights increased, and abdominal fat weight decreased. The glucose infusion rate needed to maintain euglycemia and the rate of glucose disappearance were greater in the clenbuterol-treated rats. Furthermore, plasma insulin levels were decreased, and the rate of glucose uptake into hindlimb muscles and abdominal fat was increased in the clenbuterol-treated rats. This increased rate of glucose uptake was accompanied by a parallel increase in the rate of glycogen synthesis. The increase in muscle glucose uptake could not be ascribed to an increase in the glucose transport protein GLUT-4 in clenbuterol-treated rats. We conclude that chronic clenbuterol treatment reduces the insulin resistance of the obese Zucker rat by increasing insulin-stimulated muscle and adipose tissue glucose uptake. The improvements noted may be related to the repartitioning of body weight between tissues.
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Lin, Xiaoyun, Yongnian Ni, Xueying Pei, and Serge Kokot. "Electrochemical detection of DNA damage induced by clenbuterol at a reduced graphene oxide-Nafion modified glassy carbon electrode." Analytical Methods 9, no. 7 (2017): 1105–11. http://dx.doi.org/10.1039/c6ay03022j.
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Jiang, Guang-Liang, Yu-Dong Gu, Li-Yin Zhang, Li-Ying Shen, Cong Yu, and Jian-Guang Xu. "Randomized, Double-Blind, and Placebo-Controlled Trial of Clenbuterol in Denervated Muscle Atrophy." ISRN Pharmaceutics 2011 (August 15, 2011): 1–7. http://dx.doi.org/10.5402/2011/981254.
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Objectives. β2-adrenergic agonists, such as clenbuterol, have been shown to promote the hypertrophy of healthy skeletal muscles and to ameliorate muscle wasting in a few pathological conditions in both animals and humans. We intended to investigate the clinical efficacy of clenbuterol on attenuating denervation-induced muscle atrophy. Methods. A double-blind, placebo-controlled, parallel, and randomized trial was employed. 71 patients, suffering from brachial plexus injuries, were given either clenbuterol (60 μg, bid) or placebo for 3 months. Before and at the end of the study, patients were given physical examinations, biopsies of biceps brachii, electromyograms (EMGs), and other laboratory tests. Results. Compared with placebo treatment, clenbuterol significantly mitigated the decreases in cross-sectional areas of type I and II muscle fibers and alleviated the reduction in fibrillation potential amplitudes, without any adverse effects. Conclusions. Clenbuterol safely ameliorated denervated muscle atrophy in this cohort; thus larger clinical studies are encouraged for this or other β2 agonists on denervation-induced muscle atrophy.
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Yang, Zi Jian, Tai Hu Wu, and Feng Chen. "A Portable Apparatus for Colloidal Gold Test on Clenbuterol." Advanced Materials Research 490-495 (March 2012): 3100–3104. http://dx.doi.org/10.4028/www.scientific.net/amr.490-495.3100.
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To quantitatively detect the on-site test of the content of clenbuterol in pork, a photoelectric apparatus for the colloidal gold test to detect clenbuterol was developed based on green LED and linear CCD. This design method could realize a semi-quantitative analysis of clenbuterol concentrations ranging from 0 to 1 ng/ml. Such an apparatus could promote an integrated approach to the management of the community food safety
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Rothwell, Nancy J., and Michael J. Stock. "Increased body-weight gain and body protein in castrated and adrenalectomized rats treated with clenbuterol." British Journal of Nutrition 60, no. 2 (September 1988): 355–60. http://dx.doi.org/10.1079/bjn19880105.
Full textAbstract:
1. Daily injection of the β2-adrenergic agonist clenbuterol (1 mg/kg body-weight) increased weight gain by 12% in young (35 d) male rats and by 18% in castrated rats, but had no effect on energy intake, expenditure or efficiency in either group.2. Body fat content was not affected by clenbuterol or castration, but water and protein content were significantly increased by clenbuterol treatment in both intact and castrated rats. The ratio, body protein:fat was increased by 13 and 16% in these two groups compared with their respective, untreated controls.3. Bilateral surgical adrenalectomy (ADX) of young (45 d) male rats significantly reduced body-weight, and energy intake, expenditure and efficiency. Carcass energy and fat contents were also reduced in ADX rats compared with age-matched controls.4. Clenbuterol injections stimulated weight gain (% increase: intact 15, ADX 35), and increased body protein content (% increase: intact 12, ADX 8) and the ratio, carcass protein:fat (% increase: intact 34, ADX 23).5. These findings demonstrate that the effects of clenbuterol on body-weight gain and composition in male rats occur in the absence of either gonadal or adrenal hormones. Together with other studies, these results provide further evidence to suggest that clenbuterol probably exerts its effects by a direct action on lean body mass.
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Inkster, J. E., F. D. Deb.Hovell, D. J. Kyle, D. S. Brown, and G. E. Lobley. "The effect of clenbuterol on basal protein turnover and endogenous nitrogen loss of sheep." British Journal of Nutrition 62, no. 2 (September 1989): 285–96. http://dx.doi.org/10.1079/bjn19890030.
Full textAbstract:
Seven measurements of the effect of clenbuterol on basal nitrogen excretion (UNE), and protein turnover were made in six female sheep. The sheep were sustained by the intraruminal infusion of energy as volatile fatty acids to provide maintenance, but given no protein (N-free) for 12 d (6 d control, 6 d clenbuterol). Clenbuterol reduced UNEby 20 %, but only on day 2 of the 6 d subperiod. Protein flux (equivalent to degradation on N-free nutrition), measured on day 6 by the irreversible loss of leucine was significantly increased (12%) by clenbuterol. Amino-N oxidation measured by N excretion was unchanged and, therefore, protein synthesis was also increased. During the 12 d N-free period, the recovery of urinary total N (Kjeldahl) as the sum of urea, ammonia, creatinine and purine derivatives, declined from 87.7 to 74.2 %. The form of this missing N was not identified. The effect of clenbuterol of increasing both degradation and synthesis is unlike that reported in the literature for animals receiving protein when, in general, synthesis is unchanged and degradation reduced. This could be due to a different effect of clenbuterol in the N-free state, or to unchanged effects on protein pools other than muscle whose relative contribution to protein metabolism is different in the N-free state.
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Sneddon, A. A., M. I. Delday, and C. A. Maltin. "Amelioration of denervation-induced atrophy by clenbuterol is associated with increased PKC-α activity." American Journal of Physiology-Endocrinology and Metabolism 279, no. 1 (July 1, 2000): E188—E195. http://dx.doi.org/10.1152/ajpendo.2000.279.1.e188.
Full textAbstract:
Rat soleus muscle was denervated for 3 or 7 days, and total membrane protein kinase C (PKC) activity and translocation and immunocytochemical localization of PKC isoforms were examined. Dietary administration of clenbuterol concomitant with denervation ameliorated the atrophic response and was associated with increased membrane PKC activity at both 3 (140%) and 7 (190%) days. Of the five PKC isoforms (α, ɛ, θ, ζ, and μ) detected in soleus muscle by Western immunoblotting, clenbuterol treatment affected only the PKC-α and PKC-θ forms. PKC-α was translocated to the membrane fraction upon denervation, and the presence of clenbuterol increased membrane-bound PKC-α and active PKC-α as assayed by Ser657 phosphorylation. PKC-θ protein was downregulated upon denervation, and treatment with clenbuterol further decreased both cytosolic and membrane levels. Immunolocalization of PKC-θ showed differences for regulatory and catalytic domains, with the latter showing fast-fiber type specificity. The results suggest potential roles of PKC-α and PKC-θ in the mechanism of action of clenbuterol in alleviating denervation-induced atrophy.
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McKeever, K. H., H. C. Manso Filho, E. M. Rankins, C. S. Duchamp, Y. Salah, C. K. Fenger, W. C. Duer, K. Malinowski, and G. A. Maylin. "Clenbuterol plasma concentrations after therapeutic administration in fit Standardbred horses: threshold recommendations." Comparative Exercise Physiology 17, no. 4 (June 15, 2021): 343–50. http://dx.doi.org/10.3920/cep200065.
Full textAbstract:
Clenbuterol, (RS)-1-(4-amino-3,5-dichlorophenyl)-2-(tert-butylamino)ethan-1-ol, as Ventipulmin is an FDA approved β2 agonist medication for the management of airway obstruction in horses. Administration above the FDA approved doses for clenbuterol produces repartitioning effects, which have led to restrictions on its use in human athletics and Quarter Horse and Thoroughbred racing. Clenbuterol, however has long been used therapeutically at FDA approved doses in Harness racing. The goal of this study was to identify a withdrawal time guideline for its use at FDA approvsed dose levels in Harness racing, where horses may start at seven-day intervals. Eight healthy, moderately fit Standardbred horses (4 mares, 4 geldings, weight 491±40 kg, age 13±2 years) were administered 0.8 μg/kg of clenbuterol as Ventipulmin syrup twice daily (BID) for three days. Blood samples were collected prior to dosing and at 1, 24, 48 and 96 h post administration. Clenbuterol was quantified in all samples using the New York Drug Testing and Research Laboratory ISO-17025 Racing and Medication Testing Consortium (RMTC) accredited quantitative procedure. The lower limit of quantitation of the method was 1.0 pg/ml, and three data points at 96 h post administration were censored. One horse developed diarrhoea and data from this horse was excluded from the overall analysis. Plasma regulatory thresholds were calculated using the 95/95 tolerance method and Gauss Camp Meidell at P=0.05 and P=0.001. Horses were also evaluated for effects of clenbuterol on body composition using body mass and ultrasound measurements of rump fat thickness. There were no effects (P>0.05) of clenbuterol on any of the measures including fat mass and fat free mass and thus no repartitioning effect was observed. The pharmacokinetic data and the 96 h data set support the therapeutic use of clenbuterol in Harness horses at the FDA approved 0.8 μg/kg BID dose for three days and suggest a 41 pg/ml regulatory threshold for a 96 h withdrawal time with a P=0.001 probability of randomly exceeding this regulatory threshold.
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Maltin, C. A., S. M. Hay, M. I. Delday, G. E. Lobley, and P. J. Reeds. "The action of the β-agonist clenbuterol on protein metabolism in innervated and denervated phasic muscles." Biochemical Journal 261, no. 3 (August 1, 1989): 965–71. http://dx.doi.org/10.1042/bj2610965.
Full textAbstract:
1. Clenbuterol treatment in innervated and denervated phasic extensor digitorum longus, plantaris and gastrocnemius muscles from rats caused a significant increase in RNA and protein contents in all muscles except denervated extensor digitorum longus. 2. All muscles showed an increase in the fractional rate of protein synthesis (Ks) with clenbuterol, but the temporal response varied. 3. The data suggest that the effect of clenbuterol on protein metabolism in innervated muscles is muscle-type specific, and demonstrate the homology of response for denervated muscles.
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&NA;. "Clenbuterol/heroin overdose." Reactions Weekly &NA;, no. 1234 (January 2009): 13–14. http://dx.doi.org/10.2165/00128415-200912340-00037.
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