**4. Microbiota and its role in obesity and chronic diseases**

As already described, the gut microbiota is made up of a diversity of pathogens which highlights the presence of Gram-negative or Gram-positive bacteria. The equilibrium of this ecosystem provides us great health benefits, in the absorption and digestion of nutrients, as well as influencing immune function [4–18].

In recent years, the prevalence of non-transmittable chronic diseases has increased, which has led different researchers to address the different risk factors related to the appearance of those that have been mentioned and the direct risk between microbiota and diseases [18].

Studies linked to the establishment of microbiota with chronic diseases have described that this stability of original microbiota is affected by diverse factors among which the macro- or micronutrients and dietary patterns are mentioned [18].

When the balance of microbiota is altered by a factor, whether it is the use of antibiotics, stress or diet with an increased consumption of fats, carbohydrates and fibre, it will have an effect on health. It has also been mentioned that abundance or scarcity of food, environmental pollution, chronic stress and food such as dairy products, sugars, coffee, tea and alcohol, among others, affects the intestinal mucous membrane and, consequently, changes the stability and mode of action of the microbiota [19].

All these factors cause an alteration in microbiota where the equilibrium of two large families of bacteria is affected: *Bacteroidetes* and *Firmicutes*. In a study carried out on the composition of the microbiota of obese mice, it was shown that they had increased concentrations of *Firmicutes* by more than 50%, while those of *Bacteroidetes* decreased correlatively [20].

**97**

*Gut Microbiota and Obesity: Prebiotic and Probiotic Effects*

In order to demonstrate that the microbiota changes through time, a study was carried out where old teeth found in skeletons in different periods of history were analysed. It was found that microbial changes are linked to human evolution from the hunter-gatherer period to the industrial revolution, due to the increased consumption of processed foods. These conclusions support the idea that diet and

Turnbaugh et al. carried out studies on 'humanised' or sterile mice models to which human faecal matter was transplanted and the microbiota was analysed once they were fed with a Western diet rich in fats and sugars. They found a presence of greater adiposity and a reduced proportion of *Bacteroidetes* than *Firmicutes* in the

There is a direct relationship between microbiota and energy uptake and consequently a relationship with the onset of obesity. This has been supported by a study in obese children, which showed a microbiota rich in *Enterobacteriaceae*, low in *Bacteroidetes* and increased in *Firmicutes*. When the children were subjected to diets with low carbohydrate and fat content, the composition of the microbiota

Other studies carried out in mice reflect the relationship between energy balance, diet and microbiota. The transplantation of the obese microbiota results in an increase of adiposity in the recipients, which shows that microbiota affects nutrient acquisition, energy storage and consequently the development of obesity [18, 22]. Jumpertz et al. carried out studies on the GM of obese and slim patients. They were given caloric diets, and their stools were analysed by measuring calories ingested and those eliminated in the faeces using a bomb calorimeter. This study concluded that there are changes in the GM where there are increases in energy storage, a decrease in the *Bacteroidetes* and an increase in the *Firmicutes* bacteria. All these changes could explain the variation of the uptake of energy in individuals and therefore a relationship with the predisposition to obtain metabolic disorders [18]. According to the above, the instability of the GM or changes in the original GM affects the metabolism of the whole organism. Recent studies have shown that the increase of bile acids in the intestine when comparing sterile rats with normal rats would show that the GM is not only related with obesity but also with a diverse

When transplanting GM into obese mice, the new term obesogenic microbiota was determined, associated with an increase in hepatic glucose production and promotion of triglyceride deposits. These studies show that there is an increase in TNF pro-inflammatory cytokines which can cause insulin resistance. This can be correlated with the appearance of DM-OB, since its presence has been proven to be

Toll-type receptors are receptors that recognise important patterns within immunity and inflammation processes; they are present in diabetic obese patients with metabolic syndrome. In publications made in the Latin American report, they show the role of GM with regard to the regulation of these diseases, since the mice deficient in Toll-like receptor 5 (TLR5), which recognises microbial patterns, show hyperphagia, become obese and develop characteristics indicative of metabolic syndrome. This is also proven when GM from these mice was transplanted into germ-free mice with the TLR5 gene—the receptor mice developed characteristics similar to the metabolic syndrome. In summary, Larsen et al. demonstrated that GM from diabetic patients

When administering antibiotics to these types of obese patients, many *Firmicutes*

The exact mechanisms by which GM contributes to the development of obesity have not been fully elucidated, but it has been suggested that the main ways would

directly related to the presence of elevated pro-inflammatory factors [22].

produced a significant reduction in *Firmicutes* and *Clostridia* [22, 23].

were eliminated, which resulted in improved insulin and glucose intolerance.

*DOI: http://dx.doi.org/10.5772/intechopen.86672*

the type of food alter human microbiota [18].

faecal microbiota of these mice [19].

range of metabolic diseases [21].

changed [18].

*Oral Health by Using Probiotic Products*

**Figure 1.**

status of future health of individuals.

between microbiota and diseases [18].

*Bacteroidetes* decreased correlatively [20].

fermentation of non-digestible carbohydrates, polysaccharides and oligosaccharides. It makes up an important source of energy for bacterial proliferation and produces short-chain fatty acids that the host can absorb, favouring the recovery

As well as the principal functions of GM, recent studies have associated it with the development of obesity and chronic diseases. In order to avoid such conditions, it has been proposed that the role of prebiotics and probiotics in the maintenance of

Undoubtedly, microorganisms present in the guts are fundamental throughout life as they have a direct relationship with health and illness. It is vital to take special care in the factors that make up the initial GM as it is responsible for the general

As already described, the gut microbiota is made up of a diversity of pathogens which highlights the presence of Gram-negative or Gram-positive bacteria. The equilibrium of this ecosystem provides us great health benefits, in the absorption and digestion of nutrients, as well as influencing immune function [4–18]. In recent years, the prevalence of non-transmittable chronic diseases has increased, which has led different researchers to address the different risk factors related to the appearance of those that have been mentioned and the direct risk

Studies linked to the establishment of microbiota with chronic diseases have described that this stability of original microbiota is affected by diverse factors among which the macro- or micronutrients and dietary patterns are mentioned [18]. When the balance of microbiota is altered by a factor, whether it is the use of antibiotics, stress or diet with an increased consumption of fats, carbohydrates and fibre, it will have an effect on health. It has also been mentioned that abundance or scarcity of food, environmental pollution, chronic stress and food such as dairy products, sugars, coffee, tea and alcohol, among others, affects the intestinal mucous membrane and, consequently, changes the stability and mode of action of

All these factors cause an alteration in microbiota where the equilibrium of two large families of bacteria is affected: *Bacteroidetes* and *Firmicutes*. In a study carried out on the composition of the microbiota of obese mice, it was shown that they had increased concentrations of *Firmicutes* by more than 50%, while those of

and absorption of ions such as calcium, iron and magnesium [18].

*Factors that influence the initial colonisation of gut microbiota.*

**4. Microbiota and its role in obesity and chronic diseases**

the nutritional status and prevention of diseases should be studied [4].

**96**

the microbiota [19].

In order to demonstrate that the microbiota changes through time, a study was carried out where old teeth found in skeletons in different periods of history were analysed. It was found that microbial changes are linked to human evolution from the hunter-gatherer period to the industrial revolution, due to the increased consumption of processed foods. These conclusions support the idea that diet and the type of food alter human microbiota [18].

Turnbaugh et al. carried out studies on 'humanised' or sterile mice models to which human faecal matter was transplanted and the microbiota was analysed once they were fed with a Western diet rich in fats and sugars. They found a presence of greater adiposity and a reduced proportion of *Bacteroidetes* than *Firmicutes* in the faecal microbiota of these mice [19].

There is a direct relationship between microbiota and energy uptake and consequently a relationship with the onset of obesity. This has been supported by a study in obese children, which showed a microbiota rich in *Enterobacteriaceae*, low in *Bacteroidetes* and increased in *Firmicutes*. When the children were subjected to diets with low carbohydrate and fat content, the composition of the microbiota changed [18].

Other studies carried out in mice reflect the relationship between energy balance, diet and microbiota. The transplantation of the obese microbiota results in an increase of adiposity in the recipients, which shows that microbiota affects nutrient acquisition, energy storage and consequently the development of obesity [18, 22].

Jumpertz et al. carried out studies on the GM of obese and slim patients. They were given caloric diets, and their stools were analysed by measuring calories ingested and those eliminated in the faeces using a bomb calorimeter. This study concluded that there are changes in the GM where there are increases in energy storage, a decrease in the *Bacteroidetes* and an increase in the *Firmicutes* bacteria. All these changes could explain the variation of the uptake of energy in individuals and therefore a relationship with the predisposition to obtain metabolic disorders [18].

According to the above, the instability of the GM or changes in the original GM affects the metabolism of the whole organism. Recent studies have shown that the increase of bile acids in the intestine when comparing sterile rats with normal rats would show that the GM is not only related with obesity but also with a diverse range of metabolic diseases [21].

When transplanting GM into obese mice, the new term obesogenic microbiota was determined, associated with an increase in hepatic glucose production and promotion of triglyceride deposits. These studies show that there is an increase in TNF pro-inflammatory cytokines which can cause insulin resistance. This can be correlated with the appearance of DM-OB, since its presence has been proven to be directly related to the presence of elevated pro-inflammatory factors [22].

Toll-type receptors are receptors that recognise important patterns within immunity and inflammation processes; they are present in diabetic obese patients with metabolic syndrome. In publications made in the Latin American report, they show the role of GM with regard to the regulation of these diseases, since the mice deficient in Toll-like receptor 5 (TLR5), which recognises microbial patterns, show hyperphagia, become obese and develop characteristics indicative of metabolic syndrome. This is also proven when GM from these mice was transplanted into germ-free mice with the TLR5 gene—the receptor mice developed characteristics similar to the metabolic syndrome. In summary, Larsen et al. demonstrated that GM from diabetic patients produced a significant reduction in *Firmicutes* and *Clostridia* [22, 23].

When administering antibiotics to these types of obese patients, many *Firmicutes* were eliminated, which resulted in improved insulin and glucose intolerance.

The exact mechanisms by which GM contributes to the development of obesity have not been fully elucidated, but it has been suggested that the main ways would include increased lipoprotein lipase (LPL) activity, increased intestinal permeability and lipogenesis [20]. Faecal microbiota transplantation studies in both healthy individuals and rats to obese receptors have shown the favourable action of the GM of the emitters towards the obese individuals, reducing the levels of glycemia, preventing the expansion of fat and regulating inflammatory processes. Studies also suggest that the reverse mechanism, that is, transplantation of intestinal microbiota from obese to healthy individuals, can transmit the development of obesity, assigning GM as a predisposing factor for obesity [17].

Thanks to many randomised studies that have been carried out, it will be possible to identify the microbiota properties that are contributing to the obesity epidemic, diabetes and metabolic diseases. This will in turn allow scientists to extract information and characterise diseases with the aim to prevent or cure them [21].
