Acetate-producing microbes
What this marker measures
The collective capacity of the microbial community to produce acetate, the most abundant short-chain fatty acid in the gut. Acetate supports immune function and broader metabolic regulation1–3, and can also be converted by other gut bacteria into butyrate4,5. This marker reflects the combined functional potential of all acetate-producing species, not any single organism.
Clinical associations
Consider this marker when your patient presents with:
Interpreting the result
All results are compared to Microba's healthy cohort to determine whether they fall within or outside the expected range.
Patient management insights
Support the conditions that help the entire acetate-producing community thrive.
Tips for patients discussion
Your report shows that the group of microbes responsible for producing acetate, which supports immune and metabolic health, is currently lower than expected. We can support this group by increasing specific fibres such as pectin, inulin and resistant starch.
The community
Acetate is not produced by a single species, it's a community-level function. Below are some of the most common, though this list is not exhaustive.
- Acetatifactor sp900066565
- Agathobacter rectale
- Agathobaculum butyriciproducens
- Anaerostipes hadrus
- Bacteroides thetaiotaomicron
- Bacteroides uniformis
- Bacteroides_B vulgatus
- Blautia_A massiliensis
- Blautia_A obeum
- Blautia_A wexlerae
- CAG-41 sp900066215
- Clostridium_Q sp003024715
- Clostridium_Q sp003024715
- Dorea formicigenerans
- Eubacterium_E hallii
- Faecalibacterium MIC7145
- Faecalibacterium prausnitzii_C
- Faecalibacterium prausnitzii_C
- Faecalibacterium prausnitzii_G
- Fusicatenibacter saccharivorans
- Odoribacter splanchnicus
- Odoribacter splanchnicus
- Oscillibacter sp900066435
How results are calculated
All microbiome marker results are compared against the Microba Healthy Cohort — a purpose-built group of more than 450 healthy individuals, with samples collected and analysed using the same workflow as patient samples.
Each marker is scored by comparing the patient's relative abundance against the cohort average. The distance from this average is expressed as standard deviations, and determines whether a result is classified as Low, Borderline, or High.
Source references for all clinical associations, interpretation definitions, and patient management insights on this card.
1. Xu, M. et al. Acetate attenuates inflammasome activation through GPR43-mediated Ca2+-dependent NLRP3 ubiquitination. Exp Mol Med 51, 1–13 (2019).
2. Park, J. et al. Short-chain fatty acids induce both effector and regulatory T cells by suppression of histone deacetylases and regulation of the mTOR–S6K pathway. Mucosal Immunology 8, 80–93 (2015).
3. Kimura, I. et al. The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43. Nature communications 4, 1829–1829 (2013).
4. Duncan, S. H. et al. Contribution of acetate to butyrate formation by human faecal bacteria. British Journal of Nutrition 91, 915–923 (2004).
5. Louis, P. et al. Restricted Distribution of the Butyrate Kinase Pathway among Butyrate-Producing Bacteria from the Human Colon. Journal of Bacteriology 186, 2099–2106 (2004).
6. So, D. et al. Dietary fiber intervention on gut microbiota composition in healthy adults: a systematic review and meta-analysis. Am J Clin Nutr 107, 965–983 (2018).
7. Baba, Y., Tsuge, D. & Aoki, R. Enhancement of carbohydrate metabolism by probiotic and prebiotic intake promotes short-chain fatty acid production in the gut microbiome: a randomized, double-blind, placebo-controlled crossover trial. Biosci Biotechnol Biochem 89, 1191–1202 (2025).
8. Kolida, S., Meyer, D. & Gibson, G. R. A double-blind placebo-controlled study to establish the bifidogenic dose of inulin in healthy humans. Eur J Clin Nutr 61, 1189–1195 (2007).