Leaky gut syndrome is characterized by increased intestinal permeability, translocation of compounds such as toxins, lipopolysaccharides and bacteria from the intestinal microbiota involving pro-inflammatory processes, metabolic changes, and imbalance of lipid and lipid homeotase recent research has related increased intestinal permeability to metabolic syndrome, which is characterized mainly by insulin resistance, abdominal obesity, lipid disorders, prothrombotic and pro-inflammatory processes. The objective of this study is to analyze through the literature review the pathophysiological mechanisms and factors involved in the relationship of Leaky gut syndrome and metabolic syndrome. The research included 113 scientific articles published between 2014 and 2021 in Medline/Pubmed, Scielo and Lilacs databases. Were selected, fifity original academic articles, written in English, which were analyzed according to the year of publication, evaluation method, objectives and main results. The increase in intestinal permeability and alteration of the intestinal microbiota involved inflammatory, lipidic processes, alterations in glucose homeostasis and secretion of enteroendocrine peptides among them GLUT2 and GLP-1 evidencing a strong relationship in pathophysiological mechanisms in Leaky Gut syndrome and metabolic syndrome. Even studies in humans is rare, there is an intense interrelationship between microbiota, altered intestinal permeability in Leaky Gut Syndrome and Metabolic Syndrome.

Galactosemia is an inborn error of metabolism, caused by autosomal recessive deficiency in enzymes that convert galactose to glucose. Excess galactose is converted in the liver to galactitol (alcohol of elevated toxicity), responsible for neurologic, hepatic, gastrointestinal manifestations, in varying degrees according to the mutation developed. OBJECTIVE: To observe the prevalence of galactosemia in patients with DM1 and DM2. METHODS: Group 1: patients with DM2, male gender (n=9); female gender (n=11). Group 2: patients with DM1, male gender (n=7); female gender (n=3). Group 3: Non-diabetics (n=30). Clinical follow-up of these patients included laboratory tests and imaging studies. RESULTS: There was a higher prevalence of galactosemia in DM2 patients, in comparison to DM1 patients and non-diabetics (21.66 >3.33 >1.66). The prevalence of galactosemia in DM2 patients was higher than that found in DM1 patients (2166 >3.33). CONCLUSION: Our study found a higher prevalence of galactosemia in DM2 when compared to DM1 and a healthy population.

The enteric nervous system (ENS), communicates with the central nervous system (CNS) in a dynamic and complex fashion, through different pathways forming a bidimensional axis. This balance depends on several factors, between these systems and serotonin synthesis (5 HT). The gut synthesizes about 90% of the serotonin in our body and participates in various functions such as physiological control of the energy balance and maintenance of intestinal homeostasis. However, does serotonin that is synthesized in the gut have any impact on the brain and gut? Knowledge of the relationship between the gut-brain axis and participation of the serotonin system in the control of food intake and satiety in obesity is of great interest and importance, a fascinating and growing field. Objective: To describe and analyze interactions between the Central Nervous System (CNS) and the Enteric Nervous System (ENS), related to the serotonergic mechanism in obesity. Method: A bibliographic review included data from 134 scientific articles published between 2014 and 2021 in the PubMed, SciELO, LILACS, PsycINFO and ISI Web of Knowledge databases. Results and Conclusions: Interactions between the CNS and the ENS show gastrointestinal sensory motor functions. The gut produces around 90% of serotonin in our body. However, serotonin exerts approximately 80% of its action within the gut and most of the body’s 5-HT is secreted into the bloodstream, where it is largely and rapidly eliminated by the liver and lungs. CNS serotonergic neurons are independent from ENS serotonergic neurons and enteroendocrine cells. In addition, the blood-brain barrier is impermeable to serotonin. Therefore, serotonin synthesis in the brain is one of the major mechanisms that control hunger and satiety as well as carbohydrate ingestion, some of the contributing factors in the development of obesity. Integrative medicine represents a change in paradigm from a medical view of hermetically closed compartments to an interdisciplinary view between the brain-gut axis and the serotonin mechanism in obesity.