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1.
The purpose of this study was to reveal the possible relationships between total Ca2+-dependent proteinase (CDP) and micromolar-Ca2+-dependent proteinase (microM CDP) activity and cimaterol-induced hypertrophy of skeletal muscle. Dietary administration of 10 ppm cimaterol to finishing lambs reduced microM CDP activity in longissimus muscle (LD) by 55% (P less than .01) and 70% (P less than .02) after 3 and 6 wk of treatment, respectively. Total CDP activity was unaffected by cimaterol at both treatment intervals. The reduced microM CDP activity was not associated with a reduced yield of enzyme extract from the muscle. Cimaterol treatment increased the cross-sectional area of the LD by 23.5% at 3 wk and by 35.6% at 6 wk (P less than .001). Cimaterol also increased (P less than .001) the masses of semitendinosus, semimembranosus and biceps femoris by 26%, 32.4% and 24.5%, respectively. These results suggest that cimaterol-induced muscle hypertrophy may be attained in part by reduction of myofibrillar protein degradation.  相似文献   

2.
The increased plasma glucocorticoid concentration in stressful conditions stimulates muscle protein degradation, and results in growth retardation in animals. However, the mechanism is still to be clarified. The present study was undertaken to examine the participation of Ca2+ in the glucocorticoid action, using nifedipine (NIF), a Ca2+ channel antagonist. The effects of NIF on growth, differentiation, and protein degradation were examined in glucocorticoid-treated primary cultured chick muscle cells. Muscle cell growth and cell differentiation were assessed by protein content and creatine kinase (CK) activity, respectively, and the rate of myofiblillar protein degradation was estimated by the release of N τ-methylhistidine (MeHis). Creatine kinase activity was increased by corticosterone (CTC) and this effect was minimized by NIF. Protein content was decreased by CTC and normalized by NIF. N τ-methylhistidine release was significantly increased by CTC and tended to be minimized by NIF. The present results indicate that CTC increases skeletal muscle proteolysis followed by muscle growth retardation partially because of enhanced Ca2+ influx through the NIF-sensitive Ca2+ channel. Enhanced muscle differentiation by CTC is mediated also by the NIF-sensitive Ca2+ channel.  相似文献   

3.
Expression of atrogin‐1/MAFbx, a muscle‐specific E3 ubiquitin ligase, is high under catabolic conditions, that result in muscle atrophy. Messenger RNA (mRNA) expression of atrogin‐1/MAFbx is increased by the glucocorticoid dexamethasone in mammalian skeletal muscle. This study investigated the effects of dexamethasone on expression of atrogin‐1/MAFbx in skeletal muscle of neonatal chicks and in chick myotubes. Chicks were given a single intraperitoneal injection of dexamethasone at a concentration of 10 mg/kg body weight. Twenty‐four hours after dexamethasone administration, the Pectoralis muscle weight of chicks was decreased. mRNA expression of atrogin‐1/MAFbx in skeletal muscle of chicks was significantly increased by dexamethasone administration. Expression of other proteolytic‐related genes (20S proteasome C2 subunit, m‐calpain large subunit, and cathepsin B) in skeletal muscle of chicks was not increased by dexamethasone administration. Chick myotubes were incubated with dexamethasone (1, 10 or 100 µmol/L) for 6 h. Expression of atrogin‐1/MAFbx mRNA in chick myotubes was increased in the presence of all concentrations of dexamethasone. However, expression of other proteolytic‐related genes (20S proteasome C2 subunit, m‐calpain large subunit and cathepsin B) in chick myotubes was not affected by dexamethasone treatment. These results indicate that dexamethasone enhances atrogin‐1/MAFbx expression in chick skeletal muscle, resulting in increased muscle atrophy.  相似文献   

4.
Cultures were established from neonatal rat muscle cells, satellite cells, and L6 myoblasts and changes in protein metabolism were determined as development proceeded. For all three cell types, culture protein content increased with increasing myotube content. The beta-adrenergic agonist clenbuterol (added to a final concentration of 10(-7) M) significantly stimulated fusion (as indicated by creatine kinase activity) in neonatal muscle cultures and also increased culture protein content. This was associated with a stimulation in both the fractional (ks, percentage/day, +13%, P less than .05) and absolute (As, micrograms/day, +19%, P less than .05) rates of protein synthesis within 24 h after drug administration. At 48 h, As was increased by 42% above that of controls (P less than .01). In contrast, in satellite cell cultures, clenbuterol had no consistent effects on either protein accretion, creatine kinase activity, or protein synthesis (ks and As). Similarly, the drug had no stimulatory effect on protein synthesis and protein accretion in L6 myoblast or L6 myotube cultures (and no effect in neonatally derived fibroblast cultures). It is concluded that the fusion response to clenbuterol and, therefore, changes in protein metabolism and protein accretion are greatly dependent on the origin and genetic integrity of muscle cells.  相似文献   

5.
The aim of the current study was to examine the effects of clenbuterol injection into newly hatched chicks on both the abdominal fat pad tissue weight and the skeletal muscle weight during subsequent growth. Twenty‐seven 1‐day‐old chicks were divided into two groups, receiving either a single intraperitoneal (i.p.) injection of clenbuterol (0.1 mg/kg body weight) or phosphate‐buffered saline (PBS). Body weight gain, feed intake and feed conversion ratio were not affected by clenbuterol injection during the 5‐week experimental period, while the abdominal fat pad tissue weight of the clenbuterol‐injected chicks was lower than that of the control chicks at 5 weeks post‐injection. Plasma non‐esterified fatty acid concentrations were significantly increased in the clenbuterol‐injected chicks, while plasma triacylglycerol concentrations did not differ. Additionally, the enzymatic activity of fatty acid synthase was lower in the liver of the clenbuterol‐injected chicks. Conversely, the skeletal muscle weights were not affected by clenbuterol injection. These results suggest that a single clenbuterol injection into 1‐day‐old chicks decreases the abdominal fat pad tissue weight, but may not affect skeletal muscle weights during growth. © 2015 Japanese Society of Animal Science  相似文献   

6.
Metalloproteases that selectively hydrolyze connective tissue proteins may tenderize meat without creating texture problems associated with myofibrillar protein degradation. Our objective was to characterize the activity of bovine placental proteases to determine whether they can improve meat tenderness through disruption of the connective tissue matrix. Enzymes were extracted, crudely purified, and proteolytic activity was assessed against gelatin and collagen under varying pH and temperature conditions using both SDS-PAGE and zymography. Gelatin zymography revealed proteolysis between 57 and 63 kDa, with decreased activity as buffer pH decreased from pH 7.4 to 5.4 (37 degrees C). Proteolytic activity was pronounced at 37 degrees C, moderate at 25 degrees C, and absent at 4 degrees C following 48-h incubation (pH 7.4). Placental enzymes were metalloproteases inhibited by excess EDTA. Maximum proteolysis was achieved in the presence of Ca2+, with or without Mg2+ and Zn2+. Absence of Ca2+ decreased proteolytic activity. Complete degradation of both the 125- and 120-kDa proteins of the alpha-chains of gelatin was achieved following enzyme incubation for 6 h at 37 degrees C or 24 h at 25 degrees C. No degradation was observed following enzyme incubation with native Type I collagen. Given the marked decrease in enzyme activity at pH 5.4 and 4 degrees C (standard industry conditions), bovine placental metalloproteases would not be expected to contribute to connective tissue degradation or improve meat tenderness.  相似文献   

7.
We studied the effects of exercise without or with a subsequent period on pasture on Ca2+ ATPase concentration in foal skeletal muscle, and compared the results with those previously reported on Na+, K+ ATPase. Ca2+ ATPase was measured in homogenates as Ca2+-dependent steady-state phosphorylation from [gamma-32P]ATP. From day 7 after birth, 24 foals were divided into three groups: (i) staying in a box stall (Box); (ii) staying in a box stall with an exercise programme of an increasing number of sprints per day (Exercise); and (iii) staying on pasture (Pasture). Half of the foals (12 with four in each treatment group) were killed after 5 months. The remaining foals stayed on pasture until 11 months. In the 5-month Pasture group, Ca2+ ATPase concentration was 29.4 +/- 4.3 nmol/g wet weight (wt) (n = 4) in gluteus medius muscle, 25.2 +/- 3.3 nmol/g wet wt (n = 4) in semitendinosus muscle (both mixed fibre type), and 4.1 +/- 1.7 nmol/g wet wt (n = 3) in the slow masseter muscle. These values were not altered by exercise or by box rest. This was in contrast to the Na+, K+ ATPase concentration which was not different between the three muscles, but showed a 20% rise in gluteus medius and semitendinosus muscle after exercise. In the period from 5 to 11 months on pasture, there was no change in Ca2+ ATPase in any group. In conclusion, the Ca2+ ATPase concentration in foal muscle is around 6-fold higher in mixed fibres than in slow fibres. Furthermore, the enzyme is not up- or down-regulated by sprint exercise or subsequent rest.  相似文献   

8.
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9.
对青海省大通牦牛1、30、180日龄及成年组心肌和骨骼肌线粒体Na+-K+-ATP酶、Mg2+-ATP酶、Ca2+-ATP酶和Ca2+-Mg2+-ATP酶活性进行测定。结果显示,牦牛心肌、骨骼肌线粒体Na+-K+-ATP酶、Mg2+-ATP酶、Ca2+-ATP酶和Ca2+-Mg2+-ATP酶活性在年龄组间差异均不显著(P>0.05)。表明大通牦牛在生长发育阶段心肌、骨骼肌线粒体ATP酶在物质运输、能量转换及信息传递等方面发挥着稳定的作用,且与年龄之间无明显的线性关系。  相似文献   

10.
Hydrophobic and ion-exchange chromatography were compared for yield of Ca2(+)-dependent proteases and their inhibitor in studies designed to quantify Ca2(+)-dependent proteases activity for comparative purposes. Ion-exchange (DEAE-Sephacel) proved superior to hydrophobic chromatography (Phenyl-Sepharose). Under the proper conditions, DEAE-Sephacel effectively separated low-calcium-requiring form of Ca2(+)-dependent protease (CDP-I) and CDP inhibitor. Characterization of the assay system for components of the Ca2(+)-dependent proteolytic system separated by ion-exchange chromatography indicated that proteolytic degradation of casein by Ca2(+)-dependent proteases was linear with time for up to 60 min at 25 degrees C and that it was linear up to .4 to .45 units of activity. Therefore, we recommend that, after identification of fractions containing Ca2(+)-dependent protease (CDP-I or CDP-II), these fractions be pooled, and reassayed at a volume that yields values of less than .45 units of activity. Unlike CDP-I and CDP-II, CDP inhibitor lost its activity rapidly with frozen storage (frozen in liquid nitrogen, then stored at -70 degrees C); therefore, inhibitor should be assayed in fresh (unfrozen) samples only.  相似文献   

11.
To examine the effect of a beta-adrenergic agonist (BAA) on muscle growth, proteinase activities, and postmortem proteolysis, 16 wether lambs were randomly assigned to receive 0 or 4 ppm of L644,969 in a completely mixed high-concentrate diet for 6 wk. Weight of the biceps femoris was 18.6% heavier in treated lambs. At 0 h after slaughter, treated lambs had higher cathepsin B (35.6%), cathepsins B + L (19.1%), calpastatin (62.8%), and m-calpain (24.6%) than control lambs, but both groups had similar mu-calpain activities. In both longissimus and biceps femoris muscles, treated lambs had higher protein and RNA and lower DNA concentrations. However, total DNA was not affected, indicating that the increase in muscle mass was probably due to muscle hypertrophy rather than to hyperplasia. The pattern of postmortem proteolysis was significantly altered by BAA feeding. In treated lambs, postmortem storage had no effect on the myofibril fragmentation index and degradation of desmin and troponin-T. These results indicate that the ability of the muscle to undergo postmortem proteolysis has been dramatically reduced with BAA feeding. Similar proteolytic systems are thought to be involved in antemortem and postmortem degradation of myofibrillar proteins, so BAA-mediated protein accretion is probably due, at least in part, to reduced protein degradation. To examine whether protein synthesis was altered with BAA feeding, the level of skeletal muscle alpha-actin mRNA was quantified. Longissimus muscle alpha-actin mRNA abundance was 30% greater in BAA-fed lambs. Collectively, these results indicate that dietary administration of BAA increases muscle mass through hypertrophy and that the increase in muscle protein accretion is due to reduced degradation and possibly to increased synthesis of muscle proteins.  相似文献   

12.
The effects of long-term athletic training are associated with excessive skeletal muscle turnover attributable to increased rates of myofibrillar protein synthesis and proteolysis, which are mechanisms poorly understood in the athletic dog. A physiologic field study using 44 English pointers and Labrador retrievers that had been purposely bred for bird hunting and retrieving was conducted to examine changes in the ubiquitin-proteasome (UP) pathway, which has been implicated in exercise-induced proteolysis. Muscle biopsy samples were collected from all dogs in September (preseason, pretraining) and February (peak season, peak activity). Western blot analysis was used to assess changes in expression of various components of the UP pathway in the biopsy samples. Citrate synthase and glycogen levels were also measured in a subset of these samples. Results across the population indicated pronounced up-regulation of ubiquitinated conjugates and the p31 regulatory capping subunit during the peak hunting period compared with the preseason period. In contrast, the catalytic core of the proteasome (beta-subunits) showed no apparent up-regulation in response to increased physical activity. Increased physical activity during the hunting season was associated with increased muscle glycogen levels and citrate synthase activity in these dogs. Overall, up-regulation of specific components of the UP pathway was an indication that it plays a role in the proteolytic process associated with skeletal muscle turnover during long-term athletic training, as previously believed.  相似文献   

13.
Postmortem proteolysis in skeletal muscle and factors affecting this process were examined in pork, lamb and beef longissimus muscles (LM) to determine the cause of differences in meat tenderness among these species. Fat thickness differed among species in the following order: pork greater than beef greater than lamb. The following patterns were observed for rate of temperature and pH decline: lamb greater than pork greater than beef and pork greater than beef greater than lamb, respectively. At 1 d postmortem, pork was the most tender, followed by beef and lamb, respectively. Between 1 and 14 d of postmortem storage, lamb LM was the most improved in tenderness, followed by beef and pork, respectively. Species did not differ (P greater than .05) in LM collagen solubility. Pork LM from fed pigs had the highest (P less than .05) level of cathepsins B + L and cystatin(s) activities, whereas no differences (P greater than .05) were observed among the species for cathepsin B activity. The lowest (P less than .01) Ca2(+)-dependent protease (CDP)-II and CDP inhibitor activities were observed in pork LM. Beef LM had the highest CDP inhibitor activity (P less than .05) but was intermediate in CDP-II activity. No differences were observed among species for CDP-I activity. The sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) of myofibrils isolated at 0, 1 and 14 d postmortem indicated that by d 1, desmin hydrolysis was most extensive in pork muscle, followed by lamb and beef.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

14.
The aim of the present study was to examine the signaling pathways for a low dose of angiotensin II (ANG II) on Na+ uptake of primary cultured rabbit renal proximal tubule cells (PTCs) in hormonally defined serum-free medium. The results were as follows; ANG II (10(-11) M) stimulated the proliferation of PTCs. 10(-11) M ANG II stimulated Na+ uptake by 20%, whereas 10(-9) M ANG II inhibited it by 20% (p < 0.05). The stimulatory effect of 10(-11) M ANG II on Na+ uptake was inhibited by amiloride (10(-3) M) and by losartan (ANG II receptor subtype 1 antagonist, 10(-8) M) but not by PD123319 (ANG II receptor subtype 2 antagonist, 10(-8) M). Pertussis toxin (PTX, 50 ng/ml) prevented the ANG II-induced stimulation of Na+ uptake (p < 0.01). 8-Bromoadenosine 3', 5'-cyclic monophosphate (8-Br-cAMP, 10(-6) M) did not affect Na+ uptake. SQ 22536 (adenylate cyclase inhibitor, 10(-6) M) also did not change the ANG II-induced stimulation of Na+ uptake. ANG II did not stimulate cAMP production. In contrast, 12-O-tetradecanoylphorbol-13-acetate (TPA, 0.01 ng/ml) produced significant increase in Na+ uptake. When ANG II and TPA were added together to the PTCs, there was no additive effect on Na+ uptake. Staurosporine (calcium-dependant protein kinase C inhibitor, 10(-6) M) led to a complete inhibition of ANG II-induced stimulation of Na+ uptake. ANG II-treatment resulted in a 26% increase in total protein kinase C (PKC) activity. However, 10(-11) M ANG II did not change [Ca2+]i mobilization and [3H]-AA release while 10(-9) M ANG II increased both of them. In conclusion, the PTX-sensitive PKC pathway may be the main signaling cascade in the stimulatory effects of low dose of ANG II (10(-11) M) on Na+ uptake in the primary cultured rabbit renal proximal tubule cells in hormonally defined serum-free medium.  相似文献   

15.
OBJECTIVE: To determine whether an alteration in calcium regulation by skeletal muscle sarcoplasmic reticulum, similar to known defects that cause malignant hyperthermia (MH), could be identified in membrane vesicles isolated from the muscles of Thoroughbreds with recurrent exertional rhabdomyolysis (RER). SAMPLE POPULATION: Muscle biopsy specimens from 6 Thoroughbreds with RER and 6 healthy (control) horses. PROCEDURES: RER was diagnosed on the basis of a history of > 3 episodes of exertional rhabdomyolysis confirmed by increases in serum creatine kinase (CK) activity. Skeletal muscle membrane vesicles, prepared by differential centrifugation of muscle tissue homogenates obtained from the horses, were characterized for sarcoplasmic reticulum (SR) activities, including the Ca2+ release rate for the ryanodine receptor-Ca2+ release channel, [3H]ryanodine binding activities, and rate of SR Ca2+-ATPase activity and its activation by Ca2+. RESULTS: Time course of SR Ca2+-induced Ca2+ release and [3H]ryanodine binding to the ryanodine receptor after incubation with varying concentrations of ryanodine, caffeine, and ionized calcium did not differ between muscle membranes obtained from control and RER horses. Furthermore, the maximal rate of SR Ca2+-ATPase activity and its affinity for Ca2+ did not differ between muscle membranes from control horses and horses with RER. CONCLUSIONS AND CLINICAL RELEVANCE: Despite clinical and physiologic similarities between RER and MH, we concluded that RER in Thoroughbreds does not resemble the SR ryanodine receptor defect responsible for MH and may represent a novel defect in muscle excitation-contraction coupling, calcium regulation, or contractility.  相似文献   

16.
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.  相似文献   

17.
Insulin binding to mouse adipocytes was measured after in vitro (30 min) and in vivo (5 days) exposure to clenbuterol and ractopamine. At 10(-6) M, both agonists decreased insulin binding by 20-30% after a 30 min preincubation at each insulin concentration between 1 and 25 ng/ml. Binding was not decreased if propranolol was present. Scatchard plots suggested that decreased binding was due to a decrease in insulin receptor concentration. Insulin binding was decreased approximately 10% at agonist concentrations as low as 10(-13) M, but binding was not further decreased until concentrations exceeded 10(-9) M. Rate of gain was increased 2-fold by clenbuterol (10 mg/liter of drinking water) and 50% by 500 mg ractopamine/liter, but not by 50 mg ractopamine/liter. Clenbuterol and ractopamine (500 mg/liter) decreased fat pad weight but only clenbuterol increased hind limb muscle mass. Insulin binding following in vivo administration was not influenced by ractopamine at 50 mg/liter, but tended to be increased by clenbuterol and ractopamine at 500 mg/liter. The disparity in results between administering the beta-agonists in vitro or in vivo suggests that counter regulatory factors influenced insulin binding capacity in vivo. Results indicate that ractopamine and clenbuterol can decrease insulin binding to adipocytes but the relevance of this response to decreased fat accretion is not clear.  相似文献   

18.
Clenbuterol is a beta(2)-agonist and potent selective bronchodilator that is used to treat bronchospasm in the horse. The drug is normally administered to horses orally as a syrup formulation. Once absorbed into the systemic circulation, clenbuterol has the potential to cause many side effects, including a repartitioning effect and major alterations in cardiac and skeletal muscle function. Recent studies have also reported that clenbuterol can affect bone and the immune, endocrine and reproductive systems. A great deal of information has been published on the beneficial effects of short term therapeutic doses of clenbuterol on the equine respiratory system, although there is limited information about chronic administration, particularly since this has been associated with adverse physiological effects on other systems. This review summarizes the relevant understanding of clenbuterol for clinicians and horse owners who may administer this drug to pleasure and performance horses.  相似文献   

19.
To characterize the mechanisms of acetylcholine (ACh)-induced vasorelaxation in rabbit renal arteries precontracted with high K+ (100 mM), muscle tension and cytosolic free Ca2+ concentration ([Ca2+]i) were measured simultaneously in the fura-2-loaded arterial strips. In the artery with endothelium, high K+ increased both [Ca2+]i and muscle tension. Addition of ACh (10 microM) during high-K+ induced contraction significantly relaxed the muscle and induced additional increase in [Ca2+]i. In the presence of NG-nitro-L-arginine (L-NAME, 0.1 mM). ACh increased [Ca2+]i without relaxing the muscle. In the artery without endothelium, high K+ increased both [Ca2+]i and muscle tension although ACh was ineffective, suggesting that ACh acts selectively on endothelium to increase [Ca2+]i. 4-DAMP (10 nM) or atropine (0.1 microM) abolished the ACh-induced increase in [Ca2+]i and relaxation. However, pirenzepine (0.1 microM), AF-DX 116 (1 microM) and tropicamide (1 microM) were ineffective. The ACh-induced increase of [Ca2+li and vasorelaxation was significantly reduced by 3 microM gadolinium, 10 microM lanthanum or 10 microM SKF 96365. These results suggest that, in rabbit renal artery, ACh-evoked relaxation of 100 mM K+-induced contractions is mediated by the release of endothelial NO. ACh may stimulates the M3 subtype of muscarinic receptor in the endothelial cells, resulting in the opening of the nonselective cation channels followed by an increase of [Ca2+]i and stimulation of NO synthase.  相似文献   

20.
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