Omega-3 fatty acids prevent early-life antibiotic exposure-induced gut microbiota dysbiosis and later-life obesity
Abstract
Early-life antibiotic exposure can disrupt the founding intestinal microbial community and lead to obesity later in life. Recent studies show that omega-3 fatty acids can reduce body weight gain and chronic inflammation through modulation of the gut microbiota. We hypothesize that increased tissue levels of omega-3 fatty acids may prevent antibiotic-induced alteration of gut microbiota and obesity later in life. Here, we utilize the fat-1 transgenic mouse model, which can endogenously produce omega-3 fatty acids and thereby eliminates confounding factors of diet, to show that elevated tissue levels of omega-3 fatty acids significantly reduce body weight gain and the severity of insulin resistance, fatty liver and dyslipidemia resulting from early-life exposure to azithromycin. These effects were associated with a reversal of antibiotic-induced dysbiosis of gut microbiota in fat-1 mice. These results demonstrate the beneficial effects of omega-3 fatty acids on antibiotic-induced gut dysbiosis and obesity, and suggest the potential utility of omega-3 supplementation as a safe and effective means for the prevention of obesity in children who are exposed to antibiotics.
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Early-life exposure to omega-3 prevented the onset of metabolic disorders known to be mediated through a perturbed gut microbiota profile post-antibiotic treatment.
“early-life exposure to omega-3 prevented the onset of metabolic disorders known to be mediated through a perturbed gut microbiota profile post-antibiotic treatment (Kaliannan et al., 2016).”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Kaliannan et al., 2016
The Results and Discussion (pp. 2–3) report that fat-1 mice with elevated omega-3 levels were largely protected against metabolic changes after early-life azithromycin exposure, and the paper reports associated changes in gut microbiota. But the paper describes reduced severity of some metabolic outcomes rather than complete prevention, and treats microbiota changes as an associated or proposed mechanism rather than demonstrating that they mediated the protection. (LLM, conf=0.84)
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- Authors
- Kaliannan, K., Wang, B., Li, X.-Y., Bhan, A. K., & Kang, J. X.
- Affiliations
- Harvard University (US)
- Corresponding author
- Kang, J X
- Venue
- International Journal of Obesity
- Published
- 2016-02-15
- Volume
- 40
- Issue
- 6
- Pages
- 1039-1042
- ISSN
- 0307-0565 (ISSN-L)
- 1476-5497
- OpenAlex
- W2287487780
- Cited by
- 61
- References
- 16
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 3 · 2023: 5 · 2022: 4 · 2021: 8 · 2020: 6 · 2019: 8 · 2018: 11 · 2017: 9 · 2016: 3
- FWCI
- 5.37
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- International Journal of Obesity (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- omega-3 fatty acids, early-life antibiotic exposure, gut dysbiosis, obesity, fat-1 transgenic mice, azithromycin, insulin resistance, hepatic steatosis, dyslipidemia, chronic inflammation, omega-3 supplementation, childhood obesity prevention
- MeSH terms
- Gastrointestinal Microbiome, Animals, Anti-Bacterial Agents, Disease Models, Animal, Inflammation, Male, Obesity, Weight Gain, Fatty Acids, Omega-3, Mice, Dysbiosis
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