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Review
. 2023 Jan;72(1):180-191.
doi: 10.1136/gutjnl-2022-328166. Epub 2022 Sep 28.

Advancing human gut microbiota research by considering gut transit time

Nicola Procházková  1 , Gwen Falony  2   3 , Lars Ove Dragsted  1 , Tine Rask Licht  4 , Jeroen Raes  2   3 , Henrik M Roager  5
Affiliations
Review

Advancing human gut microbiota research by considering gut transit time

Nicola Procházková et al. Gut. 2023 Jan.

Abstract

Accumulating evidence indicates that gut transit time is a key factor in shaping the gut microbiota composition and activity, which are linked to human health. Both population-wide and small-scale studies have identified transit time as a top covariate contributing to the large interindividual variation in the faecal microbiota composition. Despite this, transit time is still rarely being considered in the field of the human gut microbiome. Here, we review the latest research describing how and why whole gut and segmental transit times vary substantially between and within individuals, and how variations in gut transit time impact the gut microbiota composition, diversity and metabolism. Furthermore, we discuss the mechanisms by which the gut microbiota may causally affect gut motility. We argue that by taking into account the interindividual and intraindividual differences in gut transit time, we can advance our understanding of diet-microbiota interactions and disease-related microbiome signatures, since these may often be confounded by transient or persistent alterations in transit time. Altogether, a better understanding of the complex, bidirectional interactions between the gut microbiota and transit time is required to better understand gut microbiome variations in health and disease.

Keywords: diet; gastrointestinal physiology; gastrointestinal transit; intestinal microbiology.

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Conflict of interest statement

Competing interests: None declared.

Figures

Figure 1
Figure 1
Illustration of the complex interplay between diet, gut microbiota and gut transit time. Diet can directly affect gastrointestinal motility, especially dietary fibre and osmotically active foods can increase the faecal bulk and thereby accelerate gut transit time. Diet can also affect gut transit time by dictating the substrate availability to the gut microbiota. As a result, the gut microbiota produces metabolites such as short-chain fatty acids (SCFA), secondary bile acids, tryptamine, histamine, H2 or CH4. These microbial-derived metabolites can stimulate gastrointestinal motility and thereby impact gut transit time. In addition, gut transit time affects the gut microbial composition and metabolism and consequently the gut environment (eg, pH). The relation between the gut microbiota and the gut transit time is therefore bidirectional. In addition, host factors including gut hormones, gender, age, health status and physical activity also affect the gut transit time. GIT, gastrointestinal tract.
Figure 2
Figure 2
Segmental transit time and pH throughout the gastrointestinal tract and its association with gut environment and gut microbial metabolism. The transit time varies throughout the gastrointestinal tract with substantial interindividual differences in gastric emptying time (GET), small intestinal transit time (SITT) and colonic transit time (CTT), which account for most of the whole gut transit time. The segmental transit time ranges show the minimum and maximum transit times reported for each segment. Long gut transit time has been associated with higher faecal pH, reduced faecal water content, higher microbial cell density and diversity, and a shift in microbial metabolism from saccharolysis towards proteolysis as reflected by reduced levels of short-chain fatty acids (SCFA) and increased levels of branched-chain fatty acids (BCFA). It is likely that once easy accessible carbohydrate sources become scarce in the colon, the gut microbes switch to ferment dietary and mucin-derived proteins. While saccharolysis by the gut microbiota gives rise to SCFA that are beneficial for the host and a source of energy for the colonocytes, proteolysis can lead to the accumulation of compounds such as BCFA, phenols, indoles, ammonium (NH3) and hydrogen sulphide (H2S) that are generally considered detrimental for health. Moreover, hydrogen (H2) with carbon dioxide (CO2) or formate can be converted into methane (CH4) by methanogenic archaea, which are also linked to slower transit time. In addition, the production and circulation of secondary bile acids and hydrolysis of host-derived glucuronides excreted via bile can also be affected by alterations in gut transit time. Whether microbiota-derived trimethylamine (TMA), produced from mainly choline and carnitine, is linked to transit time remains unknown. Created with Biorender.com.
Figure 3
Figure 3
Schematic overview of microbial-derived signalling metabolites in the intestinal epithelium and their effect on gut motility. Microbial-derived metabolites interact with various metabolite receptors expressed on enterocytes or enteroendocrine cells (EEC) and stimulate serotonin secretion from the EEC cells. The released serotonin activates the enteric neurons that promote gut motility. Other metabolites (eg, histamine) can modulate gut motility via other mechanisms. 5-HT4R, serotonin receptor-4; AhR, aryl hydrocarbon receptor; FXR, Farnesoid X receptor; IAA, indoleacetic acid; IAld, indolealdehyde; ILA, indolelactic acid; SCFA, short-chain fatty acids.Created with Biorender.com.
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