Ovine carcasses were arterially infused with a volume equal to 10% of the live weight after electrical stimulation. The infusion solutions contained .075 M, .15 M or .3 M calcium chloride. Results indicated that .3 M calcium chloride treatment was the most effective concentration of CaCl2 to reduce the shear force value measured at 24 h postmortem. To examine the contribution of ionic strength to tenderization that occurs by infusion of carcasses with .3 M CaCl2, ovine carcasses were infused with CaCl2 and NaCl solutions of identical ionic strength. Results indicated that the tenderization that occurred by infusion of carcasses with CaCl2 was not due to ionic strength of the CaCl2 solution. Results also indicated that, compared to control animals, NaCl-infused carcasses were more tender after 6 d of postmortem storage (but not after 1 d, as observed with CaCl2-infused carcasses). Evidence is presented that indicates that activation of calcium-dependent proteases could be responsible for the observed tenderization (reduction in shear force) due to infusion of ovine carcasses with CaCl2.

No abstract

Several transcription factors are involved in regulating lipid metabolism in various tissues of animals. Adipocyte determination and differentiation-dependent factor 1 (ADD1), peroxisome proliferator activated receptor alpha (PPAR alpha), and peroxisome proliferator activated receptor gamma (PPAR gamma) regulate both lipogenesis and fatty acid oxidation. We determined the tissue distribution and genetic difference in mRNA concentrations of these transcription factors in two genetic populations of pigs (Newsham XL-sired Newsham Landrace x Large White Duroc and Duroc-sired US Yorkshire x Duroc-Landrace). We also determined the tissue distribution and genetic difference in the mRNA concentration of fatty acid synthase (FAS) and acyl-CoA oxidase (ACO). Our data showed that ADD1 was highly expressed in adipose tissue and liver and that mRNA concentrations of ADD1 were similar between the two genotypes. The PPAR alpha mRNA concentration was high in adipose tissue and was similar between the two genotypes. In both populations, PPAR gamma mRNA was detected only in adipose tissue. There was no difference between the two genotypes in PPAR gamma mRNA concentration. The ACO mRNA was expressed in adipose tissue, skeletal muscle, and liver with no difference between genotypes. The FAS mRNA concentration in adipose tissue was seven times higher than that in the liver. There was no detectable FAS mRNA in skeletal muscle. These data support the concept that pig adipose tissue has considerable capability for fatty acid oxidation and synthesis. The uniqueness of expression patterns for FAS and ADD1 mRNA further indicates that adipose tissue is significantly involved in fatty acid and triacylglycerol synthesis in pigs.

Much recent work has established the efficacy of certain beta-adrenergic agonists in promoting muscle growth. These compounds also lower the deposition of body lipid. Establishing whether treatment of animals with beta-adrenergic agonists alters their metabolism in ways that affect the efficiency of nutrient use will become important if these compounds are to find a place in animal production. Currently the biological basis of amino acid and energy requirements is being reexamined; this paper discusses whether we have sufficient information to conclude that the current dietary recommendations are appropriate for animals receiving beta-adrenergic agonists. When dietary protein is not a primary nutritional limitation to the rate of protein deposition, beta-adrenergic agonists should increase the efficiency with which the existing protein intake is used in growth. Alternatively, diets that supply a higher essential/nonessential amino acid ratio might be desirable. Whether additional nonprotein energy should be fed to these animals remains an open question. On one hand, the compounds increase energy expenditure and probably increase the maintenance energy needs of the recipient animals; on the other, feeding diets of higher energy density may lead to the resumption of undesirably high rates of fat deposition.