Alpha-tocopherol acetate and alpha lipoic acid may mitigate the development of wooden breast myopathy in broilers at an early age.

1. The objective of this study was to identify the effects of the antioxidant alpha-tocopherol acetate (ATA) and alpha lipoic acid (ALA) which have anti-inflammatory effects on developmental onset, severity and the progression of wooden breast (WB) based on Pectoralis major (P. major) muscle morphology and expression of genes associated with WB during the first three weeks post-hatch.2. A total of 160 newly hatched Ross 708 broiler chicks were randomly assigned in a replicated trial to either a control group or three dietary treatments (ATA 160 mg/kg feed, ALA 500 mg/kg feed or in combination).3. Microscopic changes associated with WB began at one week of age in all groups. The ATA acetate and ALA fed in combination decreased WB severity at two weeks of age (P = 0.05) and ATA alone or in combination reduced severity at three weeks of age compared to the control group (P = 0.05). Expression of myogenic determination factor 1 and peroxisome proliferator-activated receptor gamma was reduced in all dietary treatments compared to the control at three weeks of age (P ≤ 0.05), which suggested reduced muscle degeneration and lipid deposition.4. ATA and ALA fed both independently and in combination had a positive effect on mitigating WB severity microscopically as early as two weeks of age.

Effect of dietary boron on immune function in growing beef steers.

Thirty-six Angus and Angus x Simmental cross steers (initial BW 269.5 +/- 22.3 kg) were used to determine the effects of dietary boron (B) on performance and immune function. Steers were fed on one of the three dietary treatments: (i) control (no supplemental B; 7.2 mg B/kg DM), (ii) 5 mg supplemental B/kg DM and (iii) 50 mg supplemental B/kg DM, from sodium borate for 78 days. Supplementation of dietary B had no effect on body weight (BW) gain, feed intake or gain:feed during the study. Jugular blood samples were collected prior to feeding on days 28, 63 and 77 for plasma-B analysis. Supplementation of dietary B increased (p < 0.001) plasma B-concentration in a dose-responsive manner. Furthermore, plasma B-concentration was correlated (p < 0.001; R(2) = 0. 95) to daily B-intake (mg B/day). Jugular blood was also collected, from an equal number of steers from each treatment, on day 42 or 44 for determination of in vitro production of interferon-gamma and tumour necrosis factor-alpha from isolated monocytes and assessment of lymphocyte proliferation. Dietary B did not affect T- or B-lymphocyte proliferation or in vitro cytokine production from monocytes. On day 49 of the study, the humoral immune response was assessed by i.m. injection of a 25% pig red blood cell (PRBC) solution for determination of anti-PRBC IgG and IgM titre responses. Boron-supplemented steers had greater (p = 0.035) anti-PRBC IgG titres than controls on day 7 but not on day 14 or 21 post-injection. Anti-PRBC IgM titres did not differ throughout the sampling period. Results from this study indicate that supplemental B had minimal effects on immune function and did not affect performance of growing steers.

Safety evaluation of polydextrose in infant formula using a suckling piglet model.

Oligosaccharides, the third largest component in human milk, are virtually absent from cow's milk and most infant formula. Prebiotic carbohydrates like polydextrose (PDX) have been proposed as surrogates for human milk oligosaccharides. Safety assessments of novel infant formula ingredients include dose-response experiments in appropriate neonatal animal models such as the suckling pig. To further substantiate the safety of the ingredient, one-day old pigs were fed a cow's milk-based formula supplemented with PDX (1.7, 4.3, 8.5 or 17 g/L) for 18 days (n=13/dose) and compared to appropriate control (unsupplemented formula; n=13) and reference groups (day 0 pigs, and sow-reared pigs; n=13). Growth rate, formula intake, stool consistency, behavior score, blood chemistry and hematology, relative organ weights (% of body weight), tissue morphology (i.e. liver, kidney and pancreas) and pancreas biochemistry did not differ among formula-fed pigs (P>0.1). Polydextrose mimicked other prebiotic carbohydrates and had no adverse effect at the highest tested level 17.0 g PDX/L, equivalent to a dose of 8.35 g/kg of body weight per day.

Adipocytes, myofibers, and cytokine biology: new horizons in the regulation of growth and body composition.

Muscle growth in meat animals is a complex process governed by integrated signals emanating from multiple endocrine and immune cells. A generalized phenomenon among meat animal industries is that animals commonly fail to meet their genetic potential for growth in commercial production settings. Therefore, understanding the impact of stress and disease on muscle growth is essential to improving production efficiency. The adipocyte in particular seems to be well positioned as an interface between energy status and immune function, and may thus influence nutrient partitioning and growth through a combination of signals that influence fat metabolism, glucose uptake, and insulin sensitivity. Adipocytes and myofibers are active participants in the innate immune response, and as such, produce a number of metabolic regulators, including leptin, adiponectin, and proinflammatory cytokines. Specifically, adipocytes and muscle cells respond directly to bacterial lipopolysaccharide (LPS) by producing interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNFalpha). However, adipocytes are also the predominant source of the antiinflammatory hormone adiponectin, which regulates the nuclear factor kappa-B transcription factor. The ability to recognize antigens and produce regulatory molecules strategically positions adipocytes and myofibers to regulate growth locally, and to reciprocally regulate metabolism peripherally.

Cloning and expression of porcine adiponectin, and its relationship to adiposity, lipogenesis and the acute phase response.

Adiponectin is an adipocyte-derived hormone that has been implicated recently in the regulation of inflammation in immunocytes, and in lipid metabolism and glucose homeostasis in liver, skeletal muscle and adipocytes. However, information in non-rodent models is limited. We have cloned and sequenced the porcine adiponectin open reading frame and evaluated the regulation of adiponectin in vivo following lipopolysaccharide (LPS) or E. coli administration. The porcine sequence shares approximately 88, 86, 85 and 83% homology with the dog, human, cow and mouse adiponectin respectively, and 79-83% similarity with dog, human, cow and mouse proteins at the amino acid level, based on the translated porcine sequence and GenBank submissions for the other species. Relative serum adiponectin concentrations were not altered in pigs infused with E. coli, and mRNA expression in adipose tissue was not responsive to LPS. However, analysis of serum from very lean vs a substantially fatter genotype of pig indicated that relative circulating adiponectin concentrations are higher (P<0.01) in the lean pigs than in the fatter genotype, and that the difference is established relatively early in the growth curve. Also, incubating pig adipocytes for 6 h with recombinant pig adiponectin resulted in an approximately 30% reduction (P<0.05) in lipogenesis compared with adipocytes under basal conditions and with those incubated in the presence of insulin. This is the first report in any species that adiponectin antagonizes the incorporation of glucose carbon into lipid in the adipocyte, and provides additional evidence that adiponectin acts as an autocrine regulatory factor to regulate energy metabolism.

Human acylation-stimulating protein and lipid biosynthesis in bovine adipose tissue explants.

Human acylation-stimulating protein (hASP) up-regulates triacylglycerol synthesis in human adipocytes. The objectives of this research were 1) to determine the effect of hASP on triacylglycerol synthesis in bovine adipose explants and 2) to determine whether nutritional status influences the sensitivity of adipose tissue to hASP. Fresh s.c. adipose tissue was sectioned into 20- to 30-mg explants and incubated for 1 to 6 h in M199 media containing 3% BSA and either 0.75 mM [1-14C]palmitate, 0.75 mM [9, 10-3H]oleate, or 2.5 mM [1-14C] acetate, as well as hASP and(or) insulin. The explants were extracted, and lipid fractions were separated by TLC and quantified by liquid scintillation. Acetate incorporation into lipids increased 15 to 30%, and palmitate or oleate incorporation increased 10 to 25%, when explants were exposed to hASP, although this response was not significant in every experiment. Insulin increased triacylglycerol synthesis in some experiments, but not in others. Our interpretation is that acylation-stimulating protein (ASP) can mildly enhance triacylglycerol synthesis in bovine adipose tissue. To fulfill the second objective, nine 9-mo-old steers were housed individually for two periods of 3 wk each. During the first period, four of the nine steers were fed to 50% of NEm requirement and the other five consumed the same diet ad libitum. After the first period, all steers consumed feed ad libitum for 2 wk and were assigned the opposite ration for the second period. Steers gained 40.5 kg BW when allowed ad libitum access to feed but lost 30.2 kg BW when feed intake was restricted (SE = 7.84; P < 0.01). At the end of each period, s.c. adipose tissue was sectioned into explants and incubated as described above. Four explants per steer per period were used to test effects of insulin (0 and 1 nM) and hASP (0, 0.01, 0.1, and 1 microM). Insulin did not influence incorporation of acetate or oleate. Acetate incorporation (P < 0.32) was 0.99, 1.03, 1.04, and 1.10 nmol x mg(-1) h(-1) (SE = 0.13) and oleate incorporation (P < 0.01) was 0.347, 0.357, 0.353, and 0.420 nmol x mg(-1)h(-1) (SE = 0.022) for 0, 0.01, 0.1, and 1 microM hASP, respectively. Feed restriction reduced (P < 0.01) acetate and oleate incorporation by 95 and 40%, respectively. No interactions among feed intake, insulin, and hASP were detected. In conclusion, the effect of hASP on fatty acid esterification is not influenced by feed restriction.