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1. It has recently been shown that oxidative stress is involved in the pathogenesis of congestive heart failure (CHF) in broiler chickens. Vitamins E and C, common antioxidants, have been advocated for the prevention of heart failure in humans. The present study examines the effects of supplementation of these vitamins on incidence of CHF and prevention of oxidative stress in the myocardium. 2. Commercial male broilers were randomly allocated to three experimental groups and, respectively, offered commercial broiler diet (control), commercial diets fortified with vitamin E (960 IU/kg) or vitamin C (400 mg/kg). The broilers were monitored daily for overt signs of heart failure and clinical data including ECG and blood gas analysis were collected periodically. Lipid peroxidation was measured in cardiac tissues from apparently normal broilers and broilers developing CHF in each group using thiobarbituric acid reactive substances (TBARS) assay. 3. Overall, the incidence of CHF in broilers given diets fortified with vitamin E or vitamin C was not significantly different as compared to the control group. The incidence of overt signs of hypoxaemia was lower in the vitamin C group than in the control group. Lipid peroxidation was highest in broilers that developed CHF as compared to apparently normal broilers fed either vitamin E or C fortified diets. Neither vitamin E nor vitamin C was effective in preventing oxidative damage in broilers that developed CHF. 4. In conclusion, the present study confirmed that oxidative stress is involved in the pathogenesis of heart failure in broilers, but dietary supplementation of antioxidant vitamins did not prevent oxidative damage in broilers that developed CHF. Beneficial effects of vitamin C supplementation were evidenced by lower incidence of hypoxaemia, and the tendency to reduce the susceptibility of broilers to heart failure. However, vitamin E did not have any impact on clinical status or the incidence of CHF.

Early-lactating dairy cows mobilize body protein to provide amino acids that are directed toward gluconeogenesis and milk protein synthesis. Propylene glycol (PG) is a precursor of ruminal propionate, and feeding PG has been reported to improve energy supply by increasing blood glucose. Our hypothesis was that feeding PG could spare body protein by providing an alternative source of carbon for gluconeogenesis. The major objectives of this study were 1) to delineate the effects of pre- and postpartum PG supplementation in transition dairy cows on whole-body nitrogen balance, urinary 3-methylhistidine (3-MH) excretion, body composition, and gene expression profiles for the major protein degradation pathways in skeletal muscle; and 2) to characterize the changes in body protein metabolism during the periparturient period. Sixteen pregnant cows (7 primiparous and 9 multiparous) were paired based on expected calving dates and then randomly assigned within each pair to either a basal diet (control) or basal diet plus 600 mL/d of PG. Diets were fed twice daily for ad libitum intake, and PG was fed in equal amounts as a top dress from d -7 to d 45. All measurements were conducted at 3 time intervals starting at d -14 +/- 5, d 15, and d 38 relative to calving. Propylene glycol had no effect on whole-body N balance, urinary 3-MH excretion, or body composition. However, N balance was lower at d 15 and 38, compared with d -14. Urinary excretion of 3-MH was lower at d -14 than at d 15 and 38. Supplemental PG had no effect on body weight (BW) and all components of empty BW. On average, cows fed both diets mobilized 19 kg of body fat and 14 kg of body protein between d -14 and d 38. Supplemental PG had no effect on mRNA abundance in skeletal muscle for m-calpain, and the 14-kDa ubiquitin-carrier protein E2 (14-kDa E2) and proteasome 26S subunit-ATPase components of the ubiquitin-mediated proteolytic pathway; however, PG supplementation downregulated mRNA expression for mu-calpain at d 15, and tended to downregulate mRNA expression for ubiquitin at d 15 and 38. Relative to calving, mRNA abundance for m- and mu-calpain, ubiquitin, and 14-kDa E2 were greater at d 15 compared with d -14 and d 38. In summary, these results indicate that transitional effects on whole-body metabolism and gene expression for the Ca(2+)-dependent and ubiquitin-mediated proteolytic pathways in skeletal muscle were more pronounced than those elicited by PG supplementation.

Broiler diets are frequently fortified with vitamin D (D3) above the recommended levels in an attempt to prevent commonly occurring leg problems. Since the basal levels of dietary D3 are rarely known, there is a risk of over-supplementation. Over-supplementation of D3 has been shown to have detrimental effects on the heart. Sudden death syndrome (SDS) is a condition commonly observed in broiler flocks and is associated with acute heart failure. The present study examines the effects of excessive levels of vitamin D3 on cardiac health in fast growing broiler chickens. Commercial male broilers (Gallus gallus) were exposed to either a commercial diet or a commercial diet supplemented with D3. Throughout the trial all birds were monitored several times daily for overt signs of heart disease, and periodically electrocardiographic measurements were obtained. Morbidity and mortality data were collected daily. On day 32 a simulated stress challenge consisting of a single injection of epinephrine (100 microg/kg BW) was administered under continuous ECG monitoring. Broilers fed the high D3 diet were 2.5 fold more likely to succumb to acute heart failure and die of SDS (p<0.05). Electrocardiographic examination showed a higher rate of cardiac arrhythmia in birds fed the high D3 diet (22.6%), in comparison to those fed the control diet (11.8%). The stress challenge test revealed that broilers exposed to high dietary D3 were more susceptible to ventricular arrhythmia. Our findings indicate that over-supplementation of vitamin D increases the risk of SDS in broilers, and that the most likely mechanism is associated with increased susceptibility of the ventricular myocardium to arrhythmia.

The response of broiler chickens to a wide range of dietary supplementation of thiamine to broiler breeder diet was studied in order to understand the effects of maternal thiamine nutrition on the status of thiamine indices in the offspring. Thiamine, and thiamine pyrophosphate (TPP) content, and alpha-ketoglutarate dehydrogenase (KGDH) activity were measured in hearts from 20 day old chicken embryos and from chickens at 1, 7, 14, and 21 days of age and in blood at 21 days of age. Total thiamine content in the heart of day old chicks was higher in comparison to 20 day old embryos. Maternal supplementation of thiamine increased heart thiamine in the offspring (p < 0.001), and increased the activity of KGDH in the hearts of day old chicks (p < 0.001), but not in the embryo. The TPP content in the heart increased in response to both maternal and offspring thiamine supplementation (p < 0.001), however the effect of broiler thiamine supplementation was largely independent from the maternal effect. The effect of maternal thiamine nutrition on the offspring's heart KGDH activity was apparent, but the responses to broiler supplementation were dependent largely on the maternal effect. Blood TPP content was not affected by maternal thiamine supplementation (p = 0.39), but thiamine supplementation in the offspring diets increased blood TPP (p < 0.001). Both maternal and offspring thiamine supplementation increased blood free base thiamine content (both p < 0.001). It is concluded from this study that maternal thiamine nutrition affects thiamine status indices and thiamine metabolism of the offspring.