Pullets (19 wk of age) previously fed varying levels of aP (available P) with and without phytase (Natuphos) from Day 1 of age were used to determine the influence of 300 FTU phytase/kg diet on hen performance during Phase 1 (Week 21 to 36) and 2 (Week 37 to 48). At 19 wk of age, pullets were switched from developer diets to layer diets. The aP levels used in this portion of the study remained at 0.1, 0.2, 0.3, and 0.4% with and without phytase. These were the same levels fed in the starter and developer diets. Feed consumption, egg production, egg weight, egg specific gravity, and mortality were the criteria used. Reduction of aP from 0.4 to 0.2% had no effect on feed intake, egg production, egg weight, or eggshell quality (P > 0.05). However, hens fed 0.1% aP showed reduced feed intake, egg production, and bone mineral density (P < 0.001) and increased mortality (P < 0.001), but 300 FTU/kg phytase supplementation completely prevented these deficiencies. Eggs from hens fed 0.2, 0.3 and 0.4% aP diets were heavier than those fed 0.1% aP. Interactions between aP and phytase for feed consumption (P < 0.003), egg production (P < 0.001), and egg weight (P < 0.04) indicated that phytase corrected all deficiency symptoms in hens consuming 0.1% aP but showed no influence on hens fed aP levels > 0.2%. During Phase 2, aP by phytase interactions for feed consumption and egg production demonstrated that dietary phytase-corrected reductions related to P deficiency in hens consuming 0.2% aP. Results indicate that the addition of phytase in pullet diets from Day 1 of age through the first lay cycle can prevent reductions in performance of pullets fed low P diets.
Hearts isolated from 1-yr-old non-insulin-dependent diabetic rats exhibited reduced responsiveness to the beta-adrenergic agonist isoproterenol. Over a concentration range of 3 x 10(-9) to 10(-7) M, isoproterenol-mediated stimulation in the rate of left ventricular pressure decline, a measure of myocardial relaxation, and the rate of left ventricular pressure rise, a measure of myocardial contractility, were significantly depressed in the diabetic hearts. To clarify the basis for this defect, individual steps involved in the actions of the beta-adrenergic agonists were examined. Dihydroalprenolol binding assays revealed that neither beta-adrenergic receptor number nor binding affinity was affected by the diabetic condition. Also unaffected by diabetes was isoproterenol-mediated stimulation of adenylate cyclase activity, myocyte accumulation of adenosine 3',5'-cyclic monophosphate (cAMP), or the increase in cAMP-dependent protein kinase activity ratio. However, it was found that both in the presence and absence of cAMP-dependent protein kinase, activity of the sarcolemmal calcium transporter was significantly depressed in the diabetic heart. Also attenuated was protein kinase-induced enhancement of sarcoplasmic reticular calcium transport. The likelihood that these abnormalities contribute to alterations in calcium homeostasis and myocardial contractile function is discussed.
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