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Review
. 2020 Aug 5;12(8):2340.
doi: 10.3390/nu12082340.

The Relationship between Choline Bioavailability from Diet, Intestinal Microbiota Composition, and Its Modulation of Human Diseases

Affiliations
Review

The Relationship between Choline Bioavailability from Diet, Intestinal Microbiota Composition, and Its Modulation of Human Diseases

Natalia Arias et al. Nutrients. .

Abstract

Choline is a water-soluble nutrient essential for human life. Gut microbial metabolism of choline results in the production of trimethylamine (TMA), which, upon absorption by the host is converted into trimethylamine-N-oxide (TMAO) in the liver. A high accumulation of both components is related to cardiovascular disease, inflammatory bowel disease, non-alcoholic fatty liver disease, and chronic kidney disease. However, the relationship between the microbiota production of these components and its impact on these diseases still remains unknown. In this review, we will address which microbes contribute to TMA production in the human gut, the extent to which host factors (e.g., the genotype) and diet affect TMA production, and the colonization of these microbes and the reversal of dysbiosis as a therapy for these diseases.

Keywords: TMA; TMAO; cardiovascular disease (CVD); choline; chronic kidney diseases (CKD); fecal microbiota transplantation; gut microbiota; non-alcoholic steatohepatitis (NASH); polyphenols; probiotics.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the review.

Figures

Figure 1
Figure 1
Overview of choline metabolism from the diet. Choline is taken from the diet and gut microbiota trimethylamine (TMA) lyases transform it into TMA. TMA is absorbed by the intestine and delivered to the liver, where TMA is metabolized into trimethylamine N-oxide (TMAO) by host hepatic monooxygenases. Finally, TMAO is distributed to organs, where it can be eliminated (kidneys) and accumulated (tissue). However, it could cause impairment in high concentrations (cardiovascular damage, for a detailed review see Section 5).
Figure 2
Figure 2
Microorganisms involved in the metabolism of dietary choline and other trimethylamine-containing compounds. Following ingestion of foods containing choline/lecithin, or L- carnitine, certain intestinal microorganisms metabolize these compounds to trimethylamine (TMA) by different metabolic pathways. TMA can then be absorbed and transformed into trimethylamine N-oxide (TMAO) in the liver, or it can be reduced by methanogenic archaea in the gut to produce methane and ammonium.
Figure 3
Figure 3
Overview of factors affecting gut microbiota and direct effects on TMAO levels.
Figure 4
Figure 4
An overview of the ways in which choline intake may cause disease. Abbreviations: GVB, gut vascular barrier; IBD, inflammatory bowel disease; MI, myocardial infarction; NASH, non-alcoholic steatohepatitis; TMAO, trimethylamine-N-oxide.
Figure 5
Figure 5
Overview of microbiota-targeting therapies for the treatment of gastrointestinal and cardiometabolic disorders Abbreviations: FMT, fecal microbiota treatment; DMB, 3,3-Dimethyl-1-Butanol.

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