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      Effects of supplementing organic microminerals and methionine with or without limiting growth during the rearing phase of replacement gilts on lameness, growth, and body composition 1

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          Abstract

          Previous research suggested that lameness in growing pigs could be reduced using feeding strategies, such as limiting growth rate and supplementing trace minerals (TM) and (or) methionine (Met). The present study evaluates effects of 1) TM and Met and 2) limiting total lysine (Lys) during the rearing phase (90 d) of gilts (as a means to limit growth rate) on lameness, performance, and sow claw health and productivity (to first parity). Gilts ( n = 240; 58.0 ± 11.1 kg body weight [BW]) were blocked, distributed into pens of 10 gilts, and pens were allocated to a 2 × 2 factorial arrangement. Factors were: 1) control or TM plus Met, which provided additional 10, 20, and 50 mg/kg of chelated copper, manganese, and zinc, respectively (0.1%, Aplomotec Plus, Tecnología & Vitaminas, S.L.; Alforja, Spain), and a 1.01 Met:Lys ratio and 2) standard Lys was formulated to meet growth requirements or low Lys to 19% below growth requirements. Feeding was provided through two phases, first between 119 and 163 d of age (phase I) and the second between 163 and 209 d of age (phase II). Diets had 2.43 and 2.31 Mcal net energy/kg for phases I and II, respectively, and were offered ad libitum. Low Lys did not affect feed intake but rather reduced average daily gain (ADG) by 6.35% and the final BW by 3.80% compared with standard Lys ( P < 0.001). Low Lys reduced ADG ( P < 0.001) and gain:feed ( P = 0.012) during phase I but not during phase II. Lameness prevalence was 7.92% during rearing and increased with time ( P < 0.001). Final BW (151 kg) and ADG (989 g) were similar ( P > 0.05) whether gilts displayed lameness or not. Lameness was low in severity and not affected by dietary factors. However, TM- plus Met-fed gilts were 19.2 kg heavier ( P = 0.016) than were control at lameness detection. On the sow farm, there was no evidence for differences in lameness or claw lesions among previous dietary treatments. In conclusion, lameness prevalence during the rearing phase was similar, independent of TM plus Met supplement, low Lys, or the interaction. Insufficient reduction of ADG and low severity in lameness may have limited the potential of dietary treatments. Moreover, a greater deficiency of Lys would be needed to achieve the degree of growth reduction previously reported to lessen lameness through feed restriction.

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          Amino acids and immune function.

          A deficiency of dietary protein or amino acids has long been known to impair immune function and increase the susceptibility of animals and humans to infectious disease. However, only in the past 15 years have the underlying cellular and molecular mechanisms begun to unfold. Protein malnutrition reduces concentrations of most amino acids in plasma. Findings from recent studies indicate an important role for amino acids in immune responses by regulating: (1) the activation of T lymphocytes, B lymphocytes, natural killer cells and macrophages; (2) cellular redox state, gene expression and lymphocyte proliferation; and (3) the production of antibodies, cytokines and other cytotoxic substances. Increasing evidence shows that dietary supplementation of specific amino acids to animals and humans with malnutrition and infectious disease enhances the immune status, thereby reducing morbidity and mortality. Arginine, glutamine and cysteine precursors are the best prototypes. Because of a negative impact of imbalance and antagonism among amino acids on nutrient intake and utilisation, care should be exercised in developing effective strategies of enteral or parenteral provision for maximum health benefits. Such measures should be based on knowledge about the biochemistry and physiology of amino acids, their roles in immune responses, nutritional and pathological states of individuals and expected treatment outcomes. New knowledge about the metabolism of amino acids in leucocytes is critical for the development of effective means to prevent and treat immunodeficient diseases. These nutrients hold great promise in improving health and preventing infectious diseases in animals and humans.
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            Gastrointestinal functionality in animal nutrition and health: New opportunities for sustainable animal production

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              Etiology and pathogenesis of osteochondrosis.

              Osteochondrosis is a common and clinically important joint disorder that occurs in human beings and in multiple animal species, most commonly pigs, horses, and dogs. This disorder is defined as a focal disturbance of enchondral ossification and is regarded as having a multifactorial etiology, with no single factor accounting for all aspects of the disease. The most commonly cited etiologic factors are heredity, rapid growth, anatomic conformation, trauma, and dietary imbalances; however, only heredity and anatomic conformation are well supported by the scientific literature. The way in which the disease is initiated has been debated. Although formation of a fragile cartilage, failure of chondrocyte differentiation, subchondral bone necrosis, and failure of blood supply to the growth cartilage all have been proposed as the initial step in the pathogenesis, the recent literature strongly supports failure of blood supply to growth cartilage as being the most likely. The term osteochondrosis has been used to describe a wide range of different lesions among different species. We suggest a refinement of this terminology to include the modifiers latens (lesion confined to epiphyseal cartilage), manifesta (lesion accompanied by delay in endochondral ossification), and dissecans (cleft formation through articular cartilage). The purpose of this review is to provide an overview of the disease, focusing on the most commonly cited theories, recent research findings, and our own views regarding the etiology and pathogenesis of osteochondrosis, in order to provide a better understanding of this apparently complex disease.
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                Author and article information

                Journal
                Transl Anim Sci
                Transl Anim Sci
                tas
                Translational Animal Science
                Oxford University Press (US )
                2573-2102
                March 2019
                17 April 2019
                17 April 2019
                : 3
                : 2
                : 717-730
                Affiliations
                [1 ] Animal Nutrition and Welfare Service, Department of Animal and Food Science, Universitat Autònoma de Barcelona, Bellaterra, Spain
                [2 ] Department of Animal Sciences and Industry, Kansas State University, Manhattan, KS
                [3 ] Tecnología & Vitaminas S.L., Alforja, Spain
                Author notes
                Corresponding author: Lluis.Faba@ 123456uab.cat
                Author information
                http://orcid.org/0000-0002-9036-1971
                Article
                txz038
                10.1093/tas/txz038
                7200949
                fc8ea580-2421-464c-90bc-2c646773c419
                © The Author(s) 2019. Published by Oxford University Press on behalf of the American Society of Animal Science.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                : 04 December 2018
                : 15 April 2019
                Page count
                Pages: 14
                Funding
                Funded by: Centre for the Development of Industrial Technology;
                Award ID: IDI-20150749
                Categories
                Non Ruminant Nutrition
                AcademicSubjects/SCI00960

                growth,lameness,lysine,minerals,pigs
                growth, lameness, lysine, minerals, pigs

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