How did antibiotic growth promoters increase growth and feed efficiency in poultry?

Authors: MIYAKAWA, MARIANO - Instituto Nacional Tecnologia Agropecuaria; CASANOVA, NATALIA - Consejo Nacional De Investigaciones Científicas Y Técnicas(CONICET); Kogut, Michael - Mike

Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/12/2023
Publication Date: 2/2/2023
Citation: Miyakawa, M.E., Casanova, N.A., Kogut, M.H. 2023. How did antibiotic growth promoters increase growth and feed efficiency in poultry? Poultry Science. 103(2). Article 103278. https://doi.org/10.1016/j.psj.2023.103278.
DOI: https://doi.org/10.1016/j.psj.2023.103278

Interpretive Summary: For decades baby chicks were fed low levels of antibiotics which helped them grow bigger and faster; these are known as antibiotic growth promoters (AGPs). However, no one ever provided any data showing why this growth promotion was induced by the low levels of antibiotics. This paper proposes a mechanism of action of AGPs in chickens based on a number of studies reported in the literature over the last 20 years, but never evaluated as a whole. The data suggest that AGPs function by stimulating the activity of a cell structure called the mitochondria. The mitochondria are the powerhouse of all cells in the chicks' bodies because it provides most of the energy the chicks need to live and function. Understanding how AGPs work is important because more countries have now banned the use of AGPs in animal feed because of the development of high levels of antibiotic resistance found in germs associated with meat productions. Thus, there is a push to develop alternatives to antibiotics (ATAs) to improve growth in baby chicks. However, the development of ATAs has not resulted in any product that achieves the benefits of AGPs. This research is important to the poultry industry because it proposes how AGPs work and provides the framework to develop new ATAs directed towards the function of the mitochondria.

Technical 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. However, the host's ability to: (a) adapt to alterations in conditions and (b) 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 sub-therapeutic 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 have been preserved during evolution. Concordantly, gut microbiome modulation by sub-inhibitory concentration of AGPs could be the result of direct stimulation rather then 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 sub-therapeutic AGP regulation of mitochondria functional output can regulate homeostatic control mechanisms in a manner similar to those involved with disease tolerance.