Gut microbiota modulate neurobehavior through changes in brain insulin sensitivity and metabolism
Open accessAbstract
Obesity and diabetes in humans are associated with increased rates of anxiety and depression. To understand the role of the gut microbiome and brain insulin resistance in these disorders, we evaluated behaviors and insulin action in brain of mice with diet-induced obesity (DIO) with and without antibiotic treatment. We find that DIO mice have behaviors reflective of increased anxiety and depression. This is associated with decreased insulin signaling and increased inflammation in in the nucleus accumbens and amygdala. Treatment with oral metronidazole or vancomycin decreases inflammation, improves insulin signaling in the brain and reduces signs of anxiety and depression. These effects are associated with changes in the levels of tryptophan, GABA, BDNF, amino acids, and multiple acylcarnitines, and are transferable to germ-free mice by fecal transplant. Thus, changes in gut microbiota can control brain insulin signaling and metabolite levels, and this leads to altered neurobehaviors.
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Both the obese phenotype and anxiodepressive behaviors are transmissible by transplanting gut microbiota of diet-induced obese mice to normal-weight, germ-free mice.
“Notably, both the obese phenotype [73] and anxiodepressive behaviors [74] are transmissible by transplanting gut microbiota of DIO to normal-weight, germ-free mice.”
From The menace of obesity to depression and anxiety prevalence (2022) · cites this paper as [74]
Microbiota from diet-induced obese mice can weaken endothelial tight junctions and trigger inflammation in both intestine and brain and promote brain insulin resistance.
“Moreover, the microbiota from DIO mice can weaken endothelial tight junctions and trigger inflammation in both intestine and brain and promote brain insulin resistance [73,74].”
From The menace of obesity to depression and anxiety prevalence (2022) · cites this paper as [74]
It has been proposed that gut bacteria can influence neurobehavior including host appetite for food.
“It has been proposed that gut bacteria can influence neurobehavior including host appetite for food (135, 137, 182), so it is not implausible to predict associations between microbiota and all substances passing through the gut.”
From A Biopsychosocial Overview of the Opioid Crisis: Considering Nutrition and Gastrointestinal Health (2019) · cites this paper as [182]
In mice with diet-induced obesity, antibacterial treatment improves metabolic parameters, brain insulin signaling, and neurobehavioral changes indicative of anxiety and depression.
“In mice with diet-induced obesity, antibacterial treatment improved metabolic parameters, insulin signaling in the brain, and neurobehavioral changes indicative of anxiety and depression (517).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [517]
These changes are associated with altered levels of tryptophan, GABA, BDNF, amino acids, and acylcarnitines, and are transferable to germ-free mice by FMT.
“These changes were associated with altered levels of tryptophan, GABA, BDNF, amino acids, and acylcarnitines, while these effects were transferable to germ-free mice by FMT.”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [517]
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- Authors
- Soto, M., Herzog, C., Pacheco, J. A., Fujisaka, S., Bullock, K., Clish, C. B., & Kahn, C. R.
- Affiliations
- Joslin Diabetes Center (US)
- University of Toyama (JP)
- Broad Institute (US)
- Corresponding author
- Kahn, C. Ronald
- Venue
- Molecular Psychiatry
- Published
- 2018-06-18
- Volume
- 23
- Issue
- 12
- Pages
- 2287-2301
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC6294739
- OpenAlex
- W2807828439
- Cited by
- 216
- References
- 65
- Citations by year
- 2026: 15 · 2025: 19 · 2024: 21 · 2023: 23 · 2022: 33 · 2021: 32 · 2020: 38 · 2019: 28 · 2018: 7
- FWCI
- 9.33
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Molecular Psychiatry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Brigham and Women's Hospital
- Joslin Diabetes Center (DK031036)
- National Institutes of Health
- Diabetes Research Center
- Harvard Digestive Diseases Center, Harvard University
- Japan Society for the Promotion of Science (17K09821)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK055545, R37DK031036, R01DK031036, R01DK033201, P30DK036836, P30DK034854, P30DK040561)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- gut microbiota, brain insulin resistance, diet-induced obesity, anxiety, depression, neuroinflammation, metronidazole, vancomycin, antibiotic therapy, nucleus accumbens, amygdala, tryptophan, GABA, brain-derived neurotrophic factor, acylcarnitines, fecal microbiota transplantation, germ-free mice
- MeSH terms
- Gastrointestinal Microbiome, Animals, Anti-Bacterial Agents, Anxiety, Brain, Inflammation, Insulin, Insulin Resistance, Male, Metronidazole, Mice, Inbred C57BL, Obesity, RNA, Ribosomal, 16S, Vancomycin, Mice, Diet, High-Fat, Microbiota
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