Please enable JavaScript.
Coggle requires JavaScript to display documents.
Diet-Microbiota Interactions - Coggle Diagram
Diet-Microbiota Interactions
How does the diet shape the gut microbiota during different stages of life?
Infants:
Processes affecting ecological communities
Dispersal (seeding from environment)
Deterministic fitness - selection (immune system and diet)
Diversification - adaptation/mutations
Priority effects (order and timing)
Impact of delivery mode on the infant gut microbiome:
In c-section born infants
Lower amount of Bacteroides and Bifidobacterium
Higher amount of Clostridia, gram-negative and positive pathogens
Breastfeeding is associated with faster reversal of microbiome perturbations incurred after caesarean section
Antibiotics exposure delays microbiota maturation during early life
A "mature" microbiota contains certain taxa that are markers for that child's age group, whereas an "immature| or delayed microbiota resembles that of a younger child
Early exposure to antibiotics may increase the risk of allergy, asthma, atopic dermatitis BUT it depends on timing, type of antibiotics and genetics
The early gut microbiome is key for host development:
Immune development
Body growth
Appetite hormones
Nervous system
Diet has the biggest impact on the maturation of the infant gut microbiome.
Breast milk contains human milk oligosaccharides (HMOs)
-Each mother has a unique composition of HMOs --> genetic polymorphisms in genes encoding fucosyliransferases FUT2 (secretor gene)
FUT2 Genotype
Secretor (+) --> produce fucosyllated oligosaccharides
Non-secretor (-)
Two strategies in infant-associated Bifidobacterium for HMO utilisation
:
B. infantis imports HMOs inside the cytoplasm via different ABC transporters (each transporter has different affinities for different HMOs) and relies on a diverse repertoire of
intracellular glycosyl hydrolases
B. bifidum relies on a set of diverse
membrane-associated extracellular glycosyl hydrolase (GH)
Bifidobacterium species dominate the infant gut and compete for HMOs
Beastmilk vs formula milk:
Most infant formula do not currently contain HMOs
For formula milk: Some proteins (and peptides) escape digestion and absorption in the upper GI tract and reach colon where they are degraded into AAs and fermented by gut microbes --> lead to protein degrading species such as Clostridium, enterobacteriaceae
While breastmilk contain HMOs which when fermented by gut microbes result in HMO degrading Bifidobacterium species
Introducing solid foods increases alpha-diversity in infants - dietary fibres and proteins of solid foods are key
Elderly
:
Loss of diversity in the core microbiota groups is associated with increased fragility and reduced cognitive performance
Chronological age is accompanied by changes in host-microorganism homeostasis that determine, in part, the rate of physical and cognitive decline
Lifestyle and environmental effects on the microbiota can play (healthy ageing) or accelerate (unhealthy ageing) deterioration in the host and foreshorten life expectancy
Varied and healthy diet is key for microbial diversity
The more different plants you eat on a weekly basis, the higher microbial diversity
Adherence to the Mediterranean diet was associated with specific microbiome alterations
(a) enriched bacterial taxa were associated with lower fragility, improved cognition and reduced inflammatory markers
(b) increased potential for SCFA production
This can support the feasibility of improving the habitual diet to modulate the gut microbiota which in turn has the potential to promote healthier ageing
How can we modulate the gut microbiota by diet?
Habitual diet is linked to composition of the gut microbiome:
Prevotella enterotype appear to benefit from high-fibre diets
Dietary fibe and Microbiota-acessible carbohydrates
Dietary fibre (non-digestible carbohydrates)
(a) some fibres are not used by gut microbes such as cellulose, some complex fermentable carbohydrates are not defined as fibres (e.g. resistant starch)
Microbiota-accessible carbohydrates (MAC)
(a)
carbohydrates that are resistant to digestion by host metabolism, but which are metabolically available to gut microbes
(b) MACs may come from plants, fungi, animal tissues, or food-borne microbes
The human gut microbiome is estimated to encode tens of thousand soft carbohydrate-active enzymes (CAZymes)
Glycans (polysaccharides) and food-chains in the gut
Primary degraders:
Degrade glycans (such as resistant, starch, inulin, lignin, pectin, cellulose and fructo-oligosaccharides (FOS) into mono-, di- and oligosaccharides
Secondary degraders:
Capture degradation pdocuts from primary degraders and metabolise them into SCFAs
Degradation fo colonic mucus barrier enhances pathogen susceptibility:
A high-fibre diet helps to maintain mucus layer of endothelium, ensuring no gaps in the tight junctions of the endothelial cells. This prevents mucosal pathogens from entering the endothelium The high-fibre also increases finer-degrading microbiota and lower mucus-degrading microbiota.
Microbial Diversity can be confounded by colonic transit time:
It is found that a higher microbial diversity does not correlate to a healthier stool consistency
Personal responses of human microbiomes to dietary fibres:
Personal responses in butyrate concentration upon RS supplementation due to differences in the gut microbiome and specific keystone species
RS-degrading organisms (Bifidobacterium adolescents)
Increased from ~2 to 9% in enhanced/high fibre groups
Remained at ~1.5% in low group individuals
Discuss factors that may determine personal microbiome-responses to diets
Substrate availability
Metabolic capacity
Long-term changes
Abiotic factors in the gut
Host genetics (e.g. AMY1, amylase gene copy number)