## 2 Overview of the Human Gut Microbiota
### Composition and Functional Organisation of the Human Gut Microbiota
#### 2.2.1 Metabolic Functions  
The gut microbiota regulates numerous metabolic processes, including the glucose and lipid metabolisms, and contributes additional functions to the host's metabolism, such as the fermentation of non-digestible substrates (e.g., dietary fibres) and vitamin synthesis. Consequently, by participating in the digestion and fermentation processes that produce energy, the microbiota also ensures energy homeostasis [53; 54]. These processes lead to the production or modulation of metabolites by the microbiota, which act as metabolic substrates and signalling molecules, with important implications for the host health. Theseinclude trimethylamine N-oxide (TMAO) and SCFAs, such as acetate, butyrate, and propionate, derived from the fermentation of dietary fibres in the colon [53; 55].  
Several bacterial genera are involved in SCFA production. For instance, _Faecalibacterium prausnitzii_, _Roseburia_ spp., and _Eubacterium rectale_ are prominent butyrate producers, whereas _Bacteroides_ spp., _Prevolella_ spp., _Bifidobacterium_ spp., and _Ruminococcus_ spp. are key contributors to acetate and propionate synthesis [56; 57]. Butyrate and propionate are particularly vital in the regulation of glucose metabolism. They have been shown to stimulate the release of gut hormones, such as glucagon-like peptide (GLP-1) and peptide YY (PYY), which, in turn, increase satiety via the gut-brain axis and regulate blood glucose levels by increasing pancreatic insulin secretion and inhibiting glucagon production. Additionally, these SCFAs enhance glucose uptake in skeletal muscle and adipose tissue by upregulating GLUT-4 expression through AMP-activated protein kinase (AMPK) activation [58].  
The gut microbiota is also involved in the synthesis of trimethylamine (TMA) from dietary choline and L-carnitine, lecithin, phosphatidylinositol, and betaine. TMA production has been associated with species such as _Anaerococcus hydrogenalis_, _Clostridium asparagineforme_, _Clostridium hathewayi_, _Clostridium sporogenes_, _Edwardsiella tarda_, _Escherichia fergusonii_, _Proteus penneri_, and _Providencia retteri_[59; 60]. Once absorbed, TMA is transported to the liver, where it is oxidised into TMAO by hepatic flavin-containing monooxygenases, particularly FMO3. TMAO has been shown to modulate the cholesterol and bile acid metabolisms by inhibiting reverse cholesterol transport and altering bile acid synthesis and composition. These changes may promote lipid accumulation in macrophages and vascular inflammation, thereby contributing to atherosclerosis development [57; 59; 61; 62].  
Simultaneously, the gut microbiota constitutes an intrinsic source of micronutrients, including vitamins. Vitamin B biosynthesis is attributed to bacteria such as _Lactobacillus_ spp., _Bifidobacterium_ spp., _Bacteroides fragilis_, and _Escherichia coli_, which are responsible for the synthesis of water-soluble B vitamins such as biotin, riboflavin, folate, thiamine, and pantothenic acid. These contribute to microbial stability and energy metabolism by acting as coenzymes in redox reactions [63; 64; 65]. Furthermore, the gut microbiota is responsible for the synthesis of the fat-soluble vitamin K, primarily menaquinones (vitamin K2), by species such as _Enterococcus_, _Enterobacter_, _Eubacterium lentum_, _Veillonella_, and _Bacteroides_, which is essential for the activation of clotting factors and free radical neutralisation, thereby protecting cells against oxidative damage [11; 63; 66].