How did antibiotic growth promoters increase growth and feed efficiency in poultry?
- Autores
- Fernandez Miyakawa, Mariano Enrique; Casanova, Natalia Alejandra; Kogut, Michael H.
- Año de publicación
- 2024
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- 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.
Instituto de Patobiología
Fil: Fernandez Miyakawa, Mariano Enrique. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Patobiología Veterinaria; Argentina
Fil: Fernandez Miyakawa, Mariano Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Casanova, Natalia Andrea. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Patobiología Veterinaria; Argentina
Fil: Casanova, Natalia Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Kogut, Michael H. Southern Plains Agricultural Research Center; Estados Unidos - Fuente
- Poultry Science 103 (2) : 103278 (February 2024)
- Materia
-
Antibiotics
Growth Promoters
Growth
Poultry
Efficiency
Antibiótico
Promotor del Crecimiento
Crecimiento
Aves de Corral
Eficacia
Hormesis - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by-nc-sa/4.0/
- Repositorio
- Institución
- Instituto Nacional de Tecnología Agropecuaria
- OAI Identificador
- oai:localhost:20.500.12123/18516
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How did antibiotic growth promoters increase growth and feed efficiency in poultry?Fernandez Miyakawa, Mariano EnriqueCasanova, Natalia AlejandraKogut, Michael H.AntibioticsGrowth PromotersGrowthPoultryEfficiencyAntibióticoPromotor del CrecimientoCrecimientoAves de CorralEficaciaHormesisIt 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.Instituto de PatobiologíaFil: Fernandez Miyakawa, Mariano Enrique. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Patobiología Veterinaria; ArgentinaFil: Fernandez Miyakawa, Mariano Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Casanova, Natalia Andrea. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Patobiología Veterinaria; ArgentinaFil: Casanova, Natalia Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Kogut, Michael H. Southern Plains Agricultural Research Center; Estados UnidosElsevier2024-07-16T10:13:30Z2024-07-16T10:13:30Z2024-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://hdl.handle.net/20.500.12123/18516https://www.sciencedirect.com/science/article/pii/S00325791230079761525-3171https://doi.org/10.1016/j.psj.2023.103278Poultry Science 103 (2) : 103278 (February 2024)reponame:INTA Digital (INTA)instname:Instituto Nacional de Tecnología Agropecuariaenginfo:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)2025-10-16T09:31:44Zoai:localhost:20.500.12123/18516instacron:INTAInstitucionalhttp://repositorio.inta.gob.ar/Organismo científico-tecnológicoNo correspondehttp://repositorio.inta.gob.ar/oai/requesttripaldi.nicolas@inta.gob.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:l2025-10-16 09:31:45.383INTA Digital (INTA) - Instituto Nacional de Tecnología Agropecuariafalse |
dc.title.none.fl_str_mv |
How did antibiotic growth promoters increase growth and feed efficiency in poultry? |
title |
How did antibiotic growth promoters increase growth and feed efficiency in poultry? |
spellingShingle |
How did antibiotic growth promoters increase growth and feed efficiency in poultry? Fernandez Miyakawa, Mariano Enrique Antibiotics Growth Promoters Growth Poultry Efficiency Antibiótico Promotor del Crecimiento Crecimiento Aves de Corral Eficacia Hormesis |
title_short |
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_sort |
How did antibiotic growth promoters increase growth and feed efficiency in poultry? |
dc.creator.none.fl_str_mv |
Fernandez Miyakawa, Mariano Enrique Casanova, Natalia Alejandra Kogut, Michael H. |
author |
Fernandez Miyakawa, Mariano Enrique |
author_facet |
Fernandez Miyakawa, Mariano Enrique Casanova, Natalia Alejandra Kogut, Michael H. |
author_role |
author |
author2 |
Casanova, Natalia Alejandra Kogut, Michael H. |
author2_role |
author author |
dc.subject.none.fl_str_mv |
Antibiotics Growth Promoters Growth Poultry Efficiency Antibiótico Promotor del Crecimiento Crecimiento Aves de Corral Eficacia Hormesis |
topic |
Antibiotics Growth Promoters Growth Poultry Efficiency Antibiótico Promotor del Crecimiento Crecimiento Aves de Corral Eficacia Hormesis |
dc.description.none.fl_txt_mv |
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. Instituto de Patobiología Fil: Fernandez Miyakawa, Mariano Enrique. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Patobiología Veterinaria; Argentina Fil: Fernandez Miyakawa, Mariano Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Casanova, Natalia Andrea. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Patobiología Veterinaria; Argentina Fil: Casanova, Natalia Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Kogut, Michael H. Southern Plains Agricultural Research Center; Estados Unidos |
description |
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. |
publishDate |
2024 |
dc.date.none.fl_str_mv |
2024-07-16T10:13:30Z 2024-07-16T10:13:30Z 2024-02 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/20.500.12123/18516 https://www.sciencedirect.com/science/article/pii/S0032579123007976 1525-3171 https://doi.org/10.1016/j.psj.2023.103278 |
url |
http://hdl.handle.net/20.500.12123/18516 https://www.sciencedirect.com/science/article/pii/S0032579123007976 https://doi.org/10.1016/j.psj.2023.103278 |
identifier_str_mv |
1525-3171 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by-nc-sa/4.0/ Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
http://creativecommons.org/licenses/by-nc-sa/4.0/ Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Elsevier |
publisher.none.fl_str_mv |
Elsevier |
dc.source.none.fl_str_mv |
Poultry Science 103 (2) : 103278 (February 2024) reponame:INTA Digital (INTA) instname:Instituto Nacional de Tecnología Agropecuaria |
reponame_str |
INTA Digital (INTA) |
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INTA Digital (INTA) |
instname_str |
Instituto Nacional de Tecnología Agropecuaria |
repository.name.fl_str_mv |
INTA Digital (INTA) - Instituto Nacional de Tecnología Agropecuaria |
repository.mail.fl_str_mv |
tripaldi.nicolas@inta.gob.ar |
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1846143575467753472 |
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12.712165 |