Effects of a beta-adrenergic agonist (L-644,969) on performance and carcass traits of growing lambs in a cold environment

2000 ◽  
Vol 80 (3) ◽  
pp. 459-465 ◽  
Author(s):  
Y. Z. Li ◽  
R. J. Christopherson ◽  
B. T. Li ◽  
J. A. Moibi
Keyword(s):  
Nitrogen Balance ◽  
Feed Efficiency ◽  
Control Diet ◽  
Carcass Traits ◽  
Beta Agonist ◽  
Cold Environment ◽  
Adrenergic Agonist ◽  
Muscle Weight ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonist

A 2 × 2 factorial experiment was conducted to study the effects of the beta-adrenergic agonist L-644,969 (BAA, supplied at 0.28 vs. 0 mg kg−0.75 d−1) on growth performance, carcass traits and nitrogen balance of lambs at two environmental temperatures (0°C vs. 20 °C). Sixteen Suffolk-Cross wether lambs (30.2 ± 2.06 kg BW) were randomly divided into four groups and exposed to each of four experimental treatments (20 °C with control diet; 20 °C with BAA-supplemented diet; 0 °C with control diet; and 0 °C with BAA-supplemented diet) for 5 wk. The collection period for nitrogen balance was 4 d during the 4th week of treatment. The low temperature decreased efficiency of feed utilization and increased backfat thickness by 20.8% (P < 0.01) and 35.1% (P < 0.05), respectively. L-644,969, on the other hand, increased daily gain, feed efficiency and hot carcass weight by 22.5% (P < 0.05), 17.2% (P < 0.05) and 9.6% (P < 0.05,) respectively. Dressing percentage (P < 0.01), biceps femoris weight (P < 0.01) and rib eye area (P < 0.01) were also increased, but abdominal fat expressed as a percentage of liveweight (P < 0.05) was significantly decreased by BAA treatment. The improved weight gain, muscle weight and ribeye area in response to BAA, and in the absence of an increase in total nitrogen retention, indicate that the responses are due to nutrient repartitioning. Temperature did not impair the nutrient repartitioning effect of BAA, but feed efficiency may be more improved by BAA for the animals in the cold environment. Key words: Performance, carcass traits, beta-agonist, temperature, lambs

Clenbuterol-induced muscle growth: investigation of possible mediation by insulin

1987 ◽  
Vol 253 (4) ◽  
pp. E370-E375 ◽  
Author(s):  
M. A. McElligott ◽  
J. E. Mulder ◽  
L. Y. Chaung ◽  
A. Barreto
Keyword(s):  
Weight Gain ◽  
Body Weight Gain ◽  
Muscle Growth ◽  
Diabetic Rats ◽  
Normal Diet ◽  
Beta Agonist ◽  
Feed Consumption ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonist

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.

Effect of adrenergic agonists on big and small renin

1980 ◽  
Vol 238 (5) ◽  
pp. E416-E420
Author(s):  
H. Iwao ◽  
C. S. Lin ◽  
A. M. Michelakis
Keyword(s):  
Submaxillary Gland ◽  
Plasma Renin ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Molecular Weights ◽  
Submaxillary Glands ◽  
Beta Adrenergic Agonists ◽  
Beta Adrenergic Agonist ◽  
Alpha Adrenergic Agonist

The effect of alpha- and beta-adrenergic agonists on renal and submaxillary renin of different molecular weights was studied using male albino mice as experimental animals. Phenylephrine or isoproterenol was administered intravenously after removal of the submaxillary glands and/or kidneys. Renin was isolated from plasma by column chromatography and then measured by a direct radioimmunoassay. Phenylephrine increased both 68,500-dalton renin (big renin) and 38,000-dalton renin (small renin) in the plasma of nephrectomized mice. Isoproterenol increased big and small renin in the plasma of mice whose submaxillary glands were removed. In both cases, the increase of small renin was significantly greater than that of big renin. The results suggest that the alpha-adrenergic agonist phenylephrine affects the submaxillary gland, leading to the increase of both big and small plasma renin. In contrast, the beta-adrenergic agonist isoproterenol affects the kidney, leading to the increase of both big and small plasma renin.

Transforming growth factor-alpha increases alveolar liquid clearance in anesthetized ventilated rats

1996 ◽  
Vol 271 (2) ◽  
pp. L236-L244 ◽  
Author(s):  
H. G. Folkesson ◽  
J. F. Pittet ◽  
G. Nitenberg ◽  
M. A. Matthay
Keyword(s):  
Transforming Growth Factor ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Alveolar Epithelial ◽  
Factor Alpha ◽  
Beta Adrenergic Agonist ◽  
Camp Levels ◽  
Na Uptake ◽  
Alveolar Liquid Clearance ◽  
Alveolar Liquid

The effect of transforming growth factor-alpha (TGF-alpha) on alveolar liquid clearance was examined in ventilated, anesthetized rats. An isosmolar Ringer lactate solution with 10, 50, or 200 ng/ml TGF-alpha and 125I-labeled albumin as the alveolar protein tracer was instilled into the right lower lung lobe; the rats were studied for 1 and 4 h. Compared with control rats, addition of 50 ng/ml TGF-alpha to the instilled fluid increased alveolar liquid clearance by 47% over 1 h and by 66% over 4 h (P < 0.05). This increase was similar to the 50% increase in alveolar liquid clearance over 1 h in rats instilled with a beta-adrenergic agonist, salmeterol (28). There was a dose-dependent effect of TGF-alpha (10, 50, 200 ng/ml) on alveolar liquid clearance. The combination of both TGF-alpha and salmeterol did not have an additive effect on alveolar liquid clearance. The TGF-alpha-stimulated increase in alveolar liquid clearance was inhibited by amiloride (10(-4) M), indicating that the increase in clearance depended on increased Na+ uptake across the alveolar epithelium. There was only a twofold increase in intracellular cAMP levels in isolated rat alveolar epithelial type II cells after stimulation with TGF-alpha. In contrast, beta-adrenergic agonist treatment increased intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels more than tenfold. Genistein (10(-6) M), a tyrosine protein kinase inhibitor, inhibited the TGF-alpha-stimulated increase in alveolar liquid clearance. In summary, TGF-alpha can stimulate in vivo alveolar liquid clearance at a rate similar to beta-adrenergic stimulation by increasing Na+ uptake by alveolar epithelial type II cells. However, the effect may be mediated by a non-cAMP dependent mechanism. Because genistein blocked the increase in alveolar fluid clearance, the signal transduction may involve genistein-dependent phosphorylation.

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