## 1 Introduction
Regarding glucose metabolism, some _Lactobacillus_ can increase GLUT-4 expression at the muscle level, increase mRNA levels of phosphatidylinositol-3-kinase (PI3K) and insulin receptor substrate 2 (IRS2) in the liver to improve insulin sensitivity, and even reduce insulin degradation in white adipose tissue by decreasing insulin-like growth factor binding protein-3 (IGFBP-3). _Akkermans muciniphila_, _Bacteroides acidificiens_, and _Lactobacillus gasseri_ have also been found to promote fatty acid oxidation in adipose tissue and adipocyte differentiation through increased short-chain fatty acid (SCFA) synthesis and by modulating the expression of genes involved in both fatty acid oxidation and fatty acid synthesis [12]. The composition of the microbiota can vary widely depending on the anatomy, microbiological environment, and different functions of different parts of the gut. Important factors modulating its composition are host genotype, early microbial exposure during birth and lactation, as well as environmental agents such as diet. For example, diets rich in fat and protein (foods of animal origin) lead to an increase in _Firmicutes_ and _Proteobacteria_, while the intake of foods of plant origin and rich in fibre favours the growth of _Bacteroides_ and _Prerotella_. Reduced diversity of the microbiome (especially bacteria and fungi) leads to an increase in pathogenic bacteria, intestinal inflammation, and progression of metabolic diseases, such as T2 DM [10; 13]. Thus, the gut microbiota is a modulator of the'metabolic' inflammation (also called'metainflammation') observed in obesity and T2 DM, where there is an alteration in its composition (dysbiosis) [14]. In patients with T2 DM, a microbiota enriched in pathogenic species (such as _Escherichia coli_ and species of the _Clostridales_ order, such as _Clostridium_ sp.) and a decrease in the abundance of butyrate-producing bacteria, such as Bacteroides intestinals, have been found, which has a significant negative impact on metabolic homeostasis [11]. Dysbiosis alters hydrocarbon metabolism and hormone synthesis, leading to hyperglycaemia, through the synthesis of multiple metabolites, such as branched-chain amino acids (leucine, isoleucine, and valine), spermine, histamine, TMAO, etc. [15; 16; 17]. Hyperglycaemia increases intestinal permeability by altering intercellular and adhesive junctions through a GLUT-2 transporter-dependent mechanism [11; 14]; this altered integrity, in turn, favours the entry of bacterial components into the bloodstream (endotoxaemia), producing a pro-inflammatory response from the immune system. This generates what is known as 'immunometabolism', an interaction between metabolic and inflammatory pathways (such as the Toll-like receptor 4 pathway, RTL4) leading to loss of tissue functionality, with consequent \(\beta\)-pancreatic cell dysfunction, peripheral insulin resistance, and the development of fatty liver [11; 14; 16]. Similarly, the low abundance of anti-inflammatory bacteria, together with an increase in pro-inflammatory bacteria, is attributed to the occurrence and progression of T2 DM complications. An example of this is neurovascular disease, given the interaction of the microbiota with the central nervous system (CNS) through the synthesis of different neurotransmitters, neural pathways (such as the vagus nerve), and immunological pathways [8; 13]. The severity of dysbiosis is also related to the severity of the aforementioned diseases [13].