TY - JOUR
T1 - Microbiota and diabetes mellitus
T2 - Role of lipid mediators
AU - Angarita, Lissé
AU - Salazar, Juan
AU - Morillo, Valery
AU - Navarro, Carla
AU - Martínez, María Sofía
AU - Chacín, Maricarmen
AU - Torres, Wheeler
AU - Rajotia, Arush
AU - Rojas, Milagros
AU - Cano, Clímaco
AU - Añez, Roberto
AU - Rojas, Joselyn
AU - Bermudez, Valmore
N1 - Funding Information:
Funding: This work was supported by Research Grant No. CC-0437-10-21-09-10 from Consejo de Desarrollo Científico, Humanístico y Tecnológico (CONDES), University of Zulia, and Research Grant no. FZ-0058-2007 from Fundacite-Zulia.
Publisher Copyright:
© 2020 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2020/10
Y1 - 2020/10
N2 - Diabetes Mellitus (DM) is an inflammatory clinical entity with different mechanisms involved in its physiopathology. Among these, the dysfunction of the gut microbiota stands out. Currently, it is understood that lipid products derived from the gut microbiota are capable of interacting with cells from the immune system and have an immunomodulatory effect. In the presence of dysbiosis, the concentration of lipopolysaccharides (LPS) increases, favoring damage to the intestinal barrier. Furthermore, a pro-inflammatory environment prevails, and a state of insulin resistance and hyperglycemia is present. Conversely, during eubiosis, the production of short-chain fatty acids (SCFA) is fundamental for the maintenance of the integrity of the intestinal barrier as well as for immunogenic tolerance and appetite/satiety perception, leading to a protective effect. Additionally, it has been demonstrated that alterations or dysregulation of the gut microbiota can be reversed by modifying the eating habits of the patients or with the administration of prebiotics, probiotics, and symbiotics. Similarly, different studies have demonstrated that drugs like Metformin are capable of modifying the composition of the gut microbiota, promoting changes in the biosynthesis of LPS, and the metabolism of SCFA.
AB - Diabetes Mellitus (DM) is an inflammatory clinical entity with different mechanisms involved in its physiopathology. Among these, the dysfunction of the gut microbiota stands out. Currently, it is understood that lipid products derived from the gut microbiota are capable of interacting with cells from the immune system and have an immunomodulatory effect. In the presence of dysbiosis, the concentration of lipopolysaccharides (LPS) increases, favoring damage to the intestinal barrier. Furthermore, a pro-inflammatory environment prevails, and a state of insulin resistance and hyperglycemia is present. Conversely, during eubiosis, the production of short-chain fatty acids (SCFA) is fundamental for the maintenance of the integrity of the intestinal barrier as well as for immunogenic tolerance and appetite/satiety perception, leading to a protective effect. Additionally, it has been demonstrated that alterations or dysregulation of the gut microbiota can be reversed by modifying the eating habits of the patients or with the administration of prebiotics, probiotics, and symbiotics. Similarly, different studies have demonstrated that drugs like Metformin are capable of modifying the composition of the gut microbiota, promoting changes in the biosynthesis of LPS, and the metabolism of SCFA.
KW - Diabetes
KW - Dysbiosis
KW - Inflammation
KW - Lipopolysaccharides
KW - Microbiota
KW - Short-chain fatty acids
UR - http://www.scopus.com/inward/record.url?scp=85092034252&partnerID=8YFLogxK
U2 - 10.3390/nu12103039
DO - 10.3390/nu12103039
M3 - Review article
C2 - 33023000
AN - SCOPUS:85092034252
SN - 2072-6643
VL - 12
SP - 1
EP - 22
JO - Nutrients
JF - Nutrients
IS - 10
M1 - 3039
ER -