Bioaccessibility and Bioavailability of Minerals in Relation to a Healthy Gut Microbiome

Abstract

Adequate amounts of a wide range of micronutrients are needed by body tissues to maintain health. Dietary intake must be sufficient to meet these micronutrient requirements. Mineral deficiency does not seem to be the result of a physically active life or of athletic training but is more likely to arise from disturbances in the quality and quantity of ingested food. The lack of some minerals in the body appears to be symbolic of the modern era reflecting either the excessive intake of empty calories or a negative energy balance from drastic weight-loss diets. Several animal studies provide convincing evidence for an association between dietary micronutrient availability and microbial composition in the gut. However, the influence of human gut microbiota on the bioaccessibility and bioavailability of trace elements in human food has rarely been studied. Bacteria play a role by effecting mineral bioavailability and bioaccessibility, which are further increased through the fermentation of cereals and the soaking and germination of crops. Moreover, probiotics have a positive effect on iron, calcium, selenium, and zinc in relation to gut microbiome composition and metabolism. The current literature reveals the beneficial effects of bacteria on mineral bioaccessibility and bioavailability in supporting both the human gut microbiome and overall health. This review focuses on interactions between the gut microbiota and several minerals in sport nutrition, as related to a physically active lifestyle.

Keywords: Fe deficiency; gut microbiota; magnesium; micronutrient; physical fitness; trace element.

Figure 1

Bacterial strains related to mineral bioaccessibility and bioavailability. Image created according to Whisner et al. [19,20]; Amdekar et al. [21]; Aljewicz et al. [22]; Bergillos-Meca et al. [23]; Skrypnik and Suliburska [24]; Lidbeck et al. [25]; Massot-Cladera et al. [26]; Krausova et al. [27]; Malyar et al. [28] and Zhou et al. [29].

Figure 2

(A) Simplified model of iron transport via trans-cellular pathway in enterocytes. Dietary iron is absorbed on the apical side of enterocytes [E-AS] in form of ferritin, heme, or as Fe²⁺. A molecular background behind the uptake of ferritin by enterocytes is not yet clearly understood. Internalized ferritin undergoes degradation in lysosomes and Fe²⁺ is released. Endocytosis of heme is mediated by HCP1 (haem carrier protein 1). Heme is degraded in endosomes resulting in release of Fe²⁺. Nutritional iron has to be first reduced from Fe³⁺ to Fe²⁺ by ferrireductase DCYTB (duodenal cytochrome b) and it is uptaken as divalent cation by the enterocytes via DMT1 (divalent metal transporter 1), which operate in mode of Fe²⁺:H+ symporter. Recycling of H⁺ is maintained by NHE (Na⁺/H⁺ xchanger). SCFA (short chain fatty acids) produced by microbiota support the acidification on luminal side of the membrane. Fe²⁺ is exported from enterocytes on the basolateral side (E-BLS) by FPN1 (ferroportin 1). Released Fe2+ is oxidized by a transmembrane copper-dependent ferroxidase HEPH [hephaestin] to Fe3+, which is utilized by transferrin in circulation. Figure 2A was modified from Gulec et al. [85]. (B) Involvement of microbial metabolite signaling in systemic Fe homeostasis. Microbial metabolites DAP (1,3-diaminopropane) and reuterin (3-hydroxypropionaldehyde) inhibit ARNT (aryl hydro-carbon receptor nuclear translocator)–HIF-2α (transcription factor) heterodimerization/translocation. This inhibition results in downregulation of expression of DMT1, DcytB and FPN genes, which encode for the key components of Fe homeostasis and Fe²⁺ transport in enterocytes. Moreover, microbial metabolites DAP and propionate inhibit HIF-2α expression, thus influencing expression of Fe homeostatic factors/transporters.

Figure 2

(A) Simplified model of iron transport via trans-cellular pathway in enterocytes. Dietary iron is absorbed on the apical side of enterocytes [E-AS] in form of ferritin, heme, or as Fe²⁺. A molecular background behind the uptake of ferritin by enterocytes is not yet clearly understood. Internalized ferritin undergoes degradation in lysosomes and Fe²⁺ is released. Endocytosis of heme is mediated by HCP1 (haem carrier protein 1). Heme is degraded in endosomes resulting in release of Fe²⁺. Nutritional iron has to be first reduced from Fe³⁺ to Fe²⁺ by ferrireductase DCYTB (duodenal cytochrome b) and it is uptaken as divalent cation by the enterocytes via DMT1 (divalent metal transporter 1), which operate in mode of Fe²⁺:H+ symporter. Recycling of H⁺ is maintained by NHE (Na⁺/H⁺ xchanger). SCFA (short chain fatty acids) produced by microbiota support the acidification on luminal side of the membrane. Fe²⁺ is exported from enterocytes on the basolateral side (E-BLS) by FPN1 (ferroportin 1). Released Fe2+ is oxidized by a transmembrane copper-dependent ferroxidase HEPH [hephaestin] to Fe3+, which is utilized by transferrin in circulation. Figure 2A was modified from Gulec et al. [85]. (B) Involvement of microbial metabolite signaling in systemic Fe homeostasis. Microbial metabolites DAP (1,3-diaminopropane) and reuterin (3-hydroxypropionaldehyde) inhibit ARNT (aryl hydro-carbon receptor nuclear translocator)–HIF-2α (transcription factor) heterodimerization/translocation. This inhibition results in downregulation of expression of DMT1, DcytB and FPN genes, which encode for the key components of Fe homeostasis and Fe²⁺ transport in enterocytes. Moreover, microbial metabolites DAP and propionate inhibit HIF-2α expression, thus influencing expression of Fe homeostatic factors/transporters.