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Antibiotics in early life alter the murine colonic microbiome and adiposity
Open accessAbstract
Antibiotics administered in low doses have been widely used as growth promoters in the agricultural industry since the 1950s, yet the mechanisms for this effect are unclear. Because antimicrobial agents of different classes and varying activity are effective across several vertebrate species, we proposed that such subtherapeutic administration alters the population structure of the gut microbiome as well as its metabolic capabilities. We generated a model of adiposity by giving subtherapeutic antibiotic therapy to young mice and evaluated changes in the composition and capabilities of the gut microbiome. Administration of subtherapeutic antibiotic therapy increased adiposity in young mice and increased hormone levels related to metabolism. We observed substantial taxonomic changes in the microbiome, changes in copies of key genes involved in the metabolism of carbohydrates to short-chain fatty acids, increases in colonic short-chain fatty acid levels, and alterations in the regulation of hepatic metabolism of lipids and cholesterol. In this model, we demonstrate the alteration of early-life murine metabolic homeostasis through antibiotic manipulation.
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“In humans, members belonging to the Lachnospiraceae family have been shown to be protective against C. difficle (Petrof, 2013) and metabolic disorders (Cho et al., 2012).”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Cho et al., 2012
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“Subsequently, it was discovered that disruptions to the microbiome early in life can promote heightened adiposity5.”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [5]
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“In addition, by investigating the effect of early antibiotics on intestinal microbiota, a study revealed that the composition of intestinal microbiota changed significantly and the metabolism of SCFAs was altered after treatment with subtherapeutic antibiotic therapy.56”
From The role of gut dysbiosis in Parkinson’s disease: mechanistic insights and therapeutic options (2021) · cites this paper as [56]
In the citing paper
“Difficulty in maintaining new (non-native) microbiota in recipient mice, whether germ-free or those in which gut microbiota suppression was initially performed with oral mixture of poorly absorbed antibiotics, has been reported in other studies (30-32).”
From Transmission of Atherosclerosis Susceptibility with Gut Microbial Transplantation (2015) · cites this paper as [31]
In the citing paper
“The use of antibiotics in early life is associated with obesity in both people and mice”
From Diet–microbiota interactions as moderators of human metabolism (2016) · cites this paper as [66]
In the citing paper
“Several lines of evidence support the role of gut microbiota in obesity.”
From Update on Fecal Microbiota Transplantation 2015: Indications, Methodologies, Mechanisms, and Outlook (2015) · cites this paper as [80]
In the citing paper
“Lean and obese individuals show marked differences in the gut microbiome.80”
From Update on Fecal Microbiota Transplantation 2015: Indications, Methodologies, Mechanisms, and Outlook (2015) · cites this paper as [80]
In the citing paper
“antibiotic administration increases bone density in young mice (11,12)”
From Sex steroid deficiency-associated bone loss is microbiota dependent and prevented by probiotics (2016) · cites this paper as [11]
In the citing paper
“Exposure to antibiotics during weaning changed gut microbial communities with increasing metabolic capacity to produce acetate, propionate, and butyrate in C57BL/6J mice.”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [5]
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“Influx of these SCFAs to the liver resulted in substantial changes in the regulation of hepatic lipid metabolism and obese phenotype5.”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [5]
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Metadata
- Authors
- Cho, I., Yamanishi, S., Cox, L., Methé, B. A., Zavadil, J., Li, K., Gao, Z., Mahana, D., Raju, K., Teitler, I., Li, H., Alekseyenko, A. V., & Blaser, M. J.
- Affiliations
- New York University (US)
- J. Craig Venter Institute (US)
- VA NY Harbor Healthcare System (US)
- Corresponding author
- Blaser, Martin J.
- ORCID
- Venue
- Nature
- Published
- 2012-08
- Volume
- 488
- Issue
- 7413
- Pages
- 621-626
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3553221
- OpenAlex
- W2003836872
- Cited by
- 1,613
- References
- 67
- Citations by year
- 2026: 29 · 2025: 65 · 2024: 94 · 2023: 92 · 2022: 109 · 2021: 158 · 2020: 191 · 2019: 142 · 2018: 139 · 2017: 162 · 2016: 122 · 2015: 106 · 2014: 98 · 2013: 88 · 2012: 15
- FWCI
- 39.50
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Rutgers University Community Repository (Rutgers University) (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institutes of Health (UL1TR000038)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK090989, T-R01 DK090989)
- National Center for Research Resources (UL1RR029893)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Agricultural and Biological Sciences › Animal Science and Zoology › Animal Nutrition and Physiology
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- growth promoters, gut microbiota, colonic microbiota, adiposity, short-chain fatty acids, carbohydrate metabolism, lipid metabolism, cholesterol metabolism, metabolic homeostasis, livestock feed additives
- MeSH terms
- Age Factors, Animals, Anti-Bacterial Agents, Body Composition, Body Weight, Bone Development, Cecum, Cholesterol, Colon, Fatty Acids, Volatile, Feces, Female, Gastric Inhibitory Polypeptide, Liver, Male, Mice, Inbred C57BL, Weaning, Bone Density, Polymerase Chain Reaction, Adiposity, Lipid Metabolism, Mice, Metagenome
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