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Cuciniello, R.; Di Meo, F.; Filosa, S.; Crispi, S.; Bergamo, P. Microbiota Short-Chain Fatty Acids Modulate Antioxidant Defences. Encyclopedia. Available online: (accessed on 29 November 2023).
Cuciniello R, Di Meo F, Filosa S, Crispi S, Bergamo P. Microbiota Short-Chain Fatty Acids Modulate Antioxidant Defences. Encyclopedia. Available at: Accessed November 29, 2023.
Cuciniello, Rossana, Francesco Di Meo, Stefania Filosa, Stefania Crispi, Paolo Bergamo. "Microbiota Short-Chain Fatty Acids Modulate Antioxidant Defences" Encyclopedia, (accessed November 29, 2023).
Cuciniello, R., Di Meo, F., Filosa, S., Crispi, S., & Bergamo, P.(2023, June 14). Microbiota Short-Chain Fatty Acids Modulate Antioxidant Defences. In Encyclopedia.
Cuciniello, Rossana, et al. "Microbiota Short-Chain Fatty Acids Modulate Antioxidant Defences." Encyclopedia. Web. 14 June, 2023.
Microbiota Short-Chain Fatty Acids Modulate Antioxidant Defences

Food nutrients play a key role in human metabolism and health via the modulation of multiple mechanisms, including energy metabolism, intestinal homeostasis, antioxidant homeostasis, and immune responses. The intestine is an essential organ involved in human nutrition, the metabolic activity of gut microbes is essential for maintaining host health, and alterations in its composition induce metabolic shifts that may have adverse effects. The consensus on microbiota-mediated healthy effects on the host is based on the microbe-induced biotransformation of food components into bioactive metabolites. Bioactive molecules exhibit, in combination with food components, the ability to modulate the metabolic pathways of the host or to modify the composition and metabolism of the microbiota. Studies indicated the efficacy of the carbohydrates accessible to the microbiota (MACs), polyphenols, and polyunsaturated fatty acids (PUFAs) in increasing the microbial population with the ability to yield biologically active metabolites (e.g., polyphenol metabolites, short-chain fatty acids (SCFAs)) capable of modulating redox homeostasis of the host.

MACs polyphenols PUFAs gut microbiota active metabolites

1. Introduction

The beneficial effects associated with the diversity of the microbial population arise from the metabolic activities of specific microbial populations. Under eubiotic conditions, the commensal relationship between the microbiota and the host mainly consists of the capacity of bacteria to generate bioactive metabolites, starting from the ingested food, which exhibits the ability to modulate different metabolic pathways of the host [1]. For example, the production of carboxylic acids with aliphatic tails with fewer than six carbon atoms such as acetate (C2), propionate (C3), and butyrate (C4), resulting from the anaerobic fermentation of dietary plant polysaccharides, is the most relevant metabolic activity of enteric microbiota. These molecules are collectively referred to as Short-chain Fatty Acids (SCFAs) [2].

The growth of anaerobic SCFA-producing bacteria is favored by the low oxygen concentrations in the intestine where the two most abundant populations, namely, Bacteroidetes and Firmicutes, mainly produce acetate/propionate and butyrate, respectively [3]. Interestingly, due to butyrate generation during acetate metabolism, their coexistence can be consequential to mutual metabolic gain, thus resulting from the utilization of acetate produced by Bacteroidetes and Firmicutes to produce butyrate and propionate [4]. This example strongly supports the concept that the production of SCFAs is finely tuned by the balance of the bacterial species present in the gut.

The homeostatic condition of the intestinal microbiota can be restored by the level of SCFAs, and many studies in vivo describe the link between gut dysbiosis and the production of SCFAs (Table 1).
Table 1. Studies reporting the link between gut dysbiosis/production of SCFAs in several human diseases. An increase or decrease in the levels considered is indicated by upward (↑) or downward arrow (↓), respectively.
Disease Model Microbiota Alteration
Production of SCFAs
Diabetes   Randomized clinical trial
High-fiber diet
Type 2 diabetes
High fiber intake
↑ SCFA-producing bacteria
Meta analysis
Dietary fiber
↑ Butyrate, propionate
Inflammatory Bowel Disease (IBD)   313 patients ↓ Acetate-to-butyrate converter
Firmicutes (Roseburia)
↓ Propionate
↑ Pathogens (Enterobacteriaceae, Proteobacteria)
  127 patients
87 healthy controls
↓ Butyrate-producing bacteria
↓ SCFAs (acetate, propionate, butyrate)
  10 inactive Crohn patients
10 healthy controls
↓ SCFA-producing bacteria
Roseburia inulinivorans,
Ruminococcus torques,
Clostridium lavalense,
Bacteroides uniformis
Faecalibacterium prausnitzii
Nonalcoholic Fatty Liver
  14 nonalcoholic fatty liver,
18 nonalcoholic steatohepatitis
27 healthy controls
↑ SCFA levels
↑ SCFA-producing bacteria
(Fusobacteriaceae, Prevotellaceae)
  25 nonalcoholic fatty liver
25 nonalcoholic steatohepatitis
25 healthy donors
  30 patients F0/1 fibrosis stage
27 patients F ≥ 2 fibrosis
Bacteroidetes (F ≥ 2)
Ruminococcus (F ≥ 2)
Neurodegeneration Parkinson’s Disease Nonparametric meta-analysis Akkermansia
↓ Fecal SCFAs (acetate, propionate, butyrate)
96 patients
85 controls
↓ Fecal SCFAs
↑ Plasma SCFAs
↑ Pro-inflammatory bacteria
95 patients
33 controls
↓ Fecal SCFAs
(propionic acetic, butyric)
↑ Plasma SCFA
(propionic acetic)
Alzheimer’s Disease 25 patients Firmicutes, Bifidobacterium
33 dementia
22 mild cognitive impairment
120 subjective cognitive decline
↓ SCFA-producing bacteria (Ruminococcus, Eubacterium)
↑ AD biomarkers (Amyloid-β1-42 and p-tau concentrations)
Mouse model
Sodium butyrate supplementation
↓ Amyloid-β1-42 protein (40%) [18]


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