How did antibiotic growth promoters increase growth and feed efficiency in poultry?
ABSTRACT: It has been hypothesized that reducing the bioenergetic costs of gut inflammation as an explanation for the effect of antibiotic growth promoters (AGPs) on animal efficiency, framing some observations but not explaining the increase in growth rate or the prevention of infectious diseases....
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2024-02-01
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| Series: | Poultry Science |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0032579123007976 |
| _version_ | 1797317545847422976 |
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| author | Mariano Enrique Fernández Miyakawa Natalia Andrea Casanova Michael H. Kogut |
| author_facet | Mariano Enrique Fernández Miyakawa Natalia Andrea Casanova Michael H. Kogut |
| author_sort | Mariano Enrique Fernández Miyakawa |
| collection | DOAJ |
| description | ABSTRACT: It has been hypothesized that reducing the bioenergetic costs of gut inflammation as an explanation for the effect of antibiotic growth promoters (AGPs) on animal efficiency, framing some observations but not explaining the increase in growth rate or the prevention of infectious diseases. The host's ability to adapt to alterations in environmental conditions and to maintain health involves managing all physiological interactions that regulate homeostasis. Thus, metabolic pathways are vital in regulating physiological health as the energetic demands of the host guides most biological functions. Mitochondria are not only the metabolic heart of the cell because of their role in energy metabolism and oxidative phosphorylation, but also a central hub of signal transduction pathways that receive messages about the health and nutritional states of cells and tissues. In response, mitochondria direct cellular and tissue physiological alterations throughout the host. The endosymbiotic theory suggests that mitochondria evolved from prokaryotes, emphasizing the idea that these organelles can be affected by some antibiotics. Indeed, therapeutic levels of several antibiotics can be toxic to mitochondria, but subtherapeutic levels may improve mitochondrial function and defense mechanisms by inducing an adaptive response of the cell, resulting in mitokine production which coordinates an array of adaptive responses of the host to the stressor(s). This adaptive stress response is also observed in several bacteria species, suggesting that this protective mechanism has been preserved during evolution. Concordantly, gut microbiome modulation by subinhibitory concentration of AGPs could be the result of direct stimulation rather than inhibition of determined microbial species. In eukaryotes, these adaptive responses of the mitochondria to internal and external environmental conditions, can promote growth rate of the organism as an evolutionary strategy to overcome potential negative conditions. We hypothesize that direct and indirect subtherapeutic AGP regulation of mitochondria functional output can regulate homeostatic control mechanisms in a manner similar to those involved with disease tolerance. |
| first_indexed | 2024-03-08T03:36:34Z |
| format | Article |
| id | doaj.art-cbc2ed1522694a75b7f99f92d665f1a7 |
| institution | Directory Open Access Journal |
| issn | 0032-5791 |
| language | English |
| last_indexed | 2024-03-08T03:36:34Z |
| publishDate | 2024-02-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Poultry Science |
| spelling | doaj.art-cbc2ed1522694a75b7f99f92d665f1a72024-02-10T04:43:24ZengElsevierPoultry Science0032-57912024-02-011032103278How did antibiotic growth promoters increase growth and feed efficiency in poultry?Mariano Enrique Fernández Miyakawa0Natalia Andrea Casanova1Michael H. Kogut2Institute of Pathobiology, National Institute of Agricultural Technology (INTA), Argentina; National Scientific and Technical Research Council (CONICET), Buenos Aires, Argentina.; Corresponding author:Institute of Pathobiology, National Institute of Agricultural Technology (INTA), Argentina; National Scientific and Technical Research Council (CONICET), Buenos Aires, Argentina.Southern Plains Agricultural Research Center, USDA-ARS, College Station, TX, USAABSTRACT: It has been hypothesized that reducing the bioenergetic costs of gut inflammation as an explanation for the effect of antibiotic growth promoters (AGPs) on animal efficiency, framing some observations but not explaining the increase in growth rate or the prevention of infectious diseases. The host's ability to adapt to alterations in environmental conditions and to maintain health involves managing all physiological interactions that regulate homeostasis. Thus, metabolic pathways are vital in regulating physiological health as the energetic demands of the host guides most biological functions. Mitochondria are not only the metabolic heart of the cell because of their role in energy metabolism and oxidative phosphorylation, but also a central hub of signal transduction pathways that receive messages about the health and nutritional states of cells and tissues. In response, mitochondria direct cellular and tissue physiological alterations throughout the host. The endosymbiotic theory suggests that mitochondria evolved from prokaryotes, emphasizing the idea that these organelles can be affected by some antibiotics. Indeed, therapeutic levels of several antibiotics can be toxic to mitochondria, but subtherapeutic levels may improve mitochondrial function and defense mechanisms by inducing an adaptive response of the cell, resulting in mitokine production which coordinates an array of adaptive responses of the host to the stressor(s). This adaptive stress response is also observed in several bacteria species, suggesting that this protective mechanism has been preserved during evolution. Concordantly, gut microbiome modulation by subinhibitory concentration of AGPs could be the result of direct stimulation rather than inhibition of determined microbial species. In eukaryotes, these adaptive responses of the mitochondria to internal and external environmental conditions, can promote growth rate of the organism as an evolutionary strategy to overcome potential negative conditions. We hypothesize that direct and indirect subtherapeutic AGP regulation of mitochondria functional output can regulate homeostatic control mechanisms in a manner similar to those involved with disease tolerance.http://www.sciencedirect.com/science/article/pii/S0032579123007976antibiotic growth promotersgrowthproductive efficiencyhormesispoultry |
| spellingShingle | Mariano Enrique Fernández Miyakawa Natalia Andrea Casanova Michael H. Kogut How did antibiotic growth promoters increase growth and feed efficiency in poultry? Poultry Science antibiotic growth promoters growth productive efficiency hormesis poultry |
| title | How did antibiotic growth promoters increase growth and feed efficiency in poultry? |
| title_full | How did antibiotic growth promoters increase growth and feed efficiency in poultry? |
| title_fullStr | How did antibiotic growth promoters increase growth and feed efficiency in poultry? |
| title_full_unstemmed | How did antibiotic growth promoters increase growth and feed efficiency in poultry? |
| title_short | How did antibiotic growth promoters increase growth and feed efficiency in poultry? |
| title_sort | how did antibiotic growth promoters increase growth and feed efficiency in poultry |
| topic | antibiotic growth promoters growth productive efficiency hormesis poultry |
| url | http://www.sciencedirect.com/science/article/pii/S0032579123007976 |
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