Intrinsic in the equation for successful animal production is the efficiency of nutrient use for assimilation into useful animal-derived products. However, when young growing animals encounter various stressors that activate the proinflammatory response (PR), the biochemical effects of the resulting cascade of PR mediators [cytokines, prostaglandin and prosta-cyclin derivatives, nitric oxide (NO), superoxide anion (O2(.-)), etc.] override the regulatory signals normally ascribed to anabolic tissue accretion and growth. The efficiency of energy and nutrient use will proportionally decrease for growth rate due to the redirection of nutrient use to support immune defense processes. These proinflammatory events can develop in association with infectious disease but also are apparent in and a part of the natural response to birth, parturition, and weaning. If growth patterns are tracked during the PR, growth deficits are often apparent. Some growth deficits are relatively transient in duration, whereas others are quite long lasting, persisting although traditional clinical markers of PR are no longer evident. Recent evidence indicates that the PR cascades initiated by cytokines like tumor necrosis factor-alpha play a major role in these growth deficits. Perturbations in mitochondrial energetics and NO and O2(.-) interactions further affect metabolic balance. Free radicals and reactive nitrogen intermediates interact with select molecular targets in proteins (i.e., enzymes, histone proteins, and signal transduction proteins), causing the nitration and nitrosylation of select amino acids. If these posttranslational modifications occur in proteins associated with control points critical in metabolic stability, the resulting altered protein structure blocks its functionality. Attenuation of these overt posttranslational protein modifications at their site of production offers a strategy to minimize their detrimental impact while preserving needed cytokine, NO, and O2(.-) functions.

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Trace mineral status was evaluated in a 2 x 3 factorial treatment array with a total of 34 barrows growing from 25 to 55 kg live weight. Treatments included three levels of feed intake (100, 80 and 60% of ad libitum intake) and exogenous pituitary growth hormone (pGH) therapy (0 and 100 micrograms/kg BW daily). Blood was collected prior to slaughter for the determination of hematocrit and serum trace metal concentrations; tissues (liver, heart, kidney, bone and muscle) were obtained when pigs were slaughtered at 55 kg. Hematocrits and serum Fe were lower in pGH-treated pigs than in controls at all levels of feed intake. Serum Cu was increased by feed restriction but was not altered by pGH therapy. The concentration of serum Zn was not affected by either treatment. Concentrations of hepatic Fe and Cu were lower in pGH-treated pigs than in controls but were higher in feed-restricted pigs than in ad libitum-fed pigs. However, the total amounts of hepatic Fe and Cu were similar in pGH-treated pigs to concentrations in controls. The concentration of hepatic Zn was not influenced by either pGH treatment or feed intake. Femur weights were marginally greater in pGH-treated pigs, probably due to elevated water content. Iron concentration in bone was higher in pGH-treated pigs than in control pigs, whereas Ca, Cu and Zn were not influenced by pGH treatment or feed restriction. Feed intake and pGH treatment did not influence the concentrations of Fe, Cu or Zn in muscle. These findings indicate that pGH therapy affects the metabolism of Fe but has little impact on the overall composition of body ash.