Microbiota and Diabetes Mellitus: Role of Lipid Mediators
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 fr...
- Autores:
-
Salazar, Juan
Angarita, Lissé
Morillo, Valery
Navarro, Carla
Martínez, María Sofía
Chacín, Maricarmen
Torres, Wheeler
Rajotia, Arush
Rojas, Milagros
Cano, Clímaco
Añez, Roberto
Rojas, Joselyn
Bermúdez, Valmore
- Tipo de recurso:
- Fecha de publicación:
- 2020
- Institución:
- Universidad Simón Bolívar
- Repositorio:
- Repositorio Digital USB
- Idioma:
- eng
- OAI Identifier:
- oai:bonga.unisimon.edu.co:20.500.12442/7003
- Acceso en línea:
- https://hdl.handle.net/20.500.12442/7003
https://doi.org/10.3390/nu12103039
https://www.mdpi.com/2072-6643/12/10/3039
- Palabra clave:
- Diabetes
Inflammation
Microbiota
Dysbiosis
Lipopolysaccharides
Short-chain
Fatty acids
- Rights
- openAccess
- License
- Attribution-NonCommercial-NoDerivatives 4.0 Internacional
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dc.title.eng.fl_str_mv |
Microbiota and Diabetes Mellitus: Role of Lipid Mediators |
title |
Microbiota and Diabetes Mellitus: Role of Lipid Mediators |
spellingShingle |
Microbiota and Diabetes Mellitus: Role of Lipid Mediators Diabetes Inflammation Microbiota Dysbiosis Lipopolysaccharides Short-chain Fatty acids |
title_short |
Microbiota and Diabetes Mellitus: Role of Lipid Mediators |
title_full |
Microbiota and Diabetes Mellitus: Role of Lipid Mediators |
title_fullStr |
Microbiota and Diabetes Mellitus: Role of Lipid Mediators |
title_full_unstemmed |
Microbiota and Diabetes Mellitus: Role of Lipid Mediators |
title_sort |
Microbiota and Diabetes Mellitus: Role of Lipid Mediators |
dc.creator.fl_str_mv |
Salazar, Juan Angarita, Lissé Morillo, Valery Navarro, Carla Martínez, María Sofía Chacín, Maricarmen Torres, Wheeler Rajotia, Arush Rojas, Milagros Cano, Clímaco Añez, Roberto Rojas, Joselyn Bermúdez, Valmore |
dc.contributor.author.none.fl_str_mv |
Salazar, Juan Angarita, Lissé Morillo, Valery Navarro, Carla Martínez, María Sofía Chacín, Maricarmen Torres, Wheeler Rajotia, Arush Rojas, Milagros Cano, Clímaco Añez, Roberto Rojas, Joselyn Bermúdez, Valmore |
dc.subject.spa.fl_str_mv |
Diabetes |
topic |
Diabetes Inflammation Microbiota Dysbiosis Lipopolysaccharides Short-chain Fatty acids |
dc.subject.eng.fl_str_mv |
Inflammation Microbiota Dysbiosis Lipopolysaccharides Short-chain Fatty acids |
description |
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. |
publishDate |
2020 |
dc.date.issued.none.fl_str_mv |
2020 |
dc.date.accessioned.none.fl_str_mv |
2021-01-20T23:07:35Z |
dc.date.available.none.fl_str_mv |
2021-01-20T23:07:35Z |
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http://purl.org/coar/version/c_970fb48d4fbd8a85 |
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Artículo científico |
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20726643 |
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https://hdl.handle.net/20.500.12442/7003 |
dc.identifier.doi.none.fl_str_mv |
https://doi.org/10.3390/nu12103039 |
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https://www.mdpi.com/2072-6643/12/10/3039 |
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20726643 |
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https://hdl.handle.net/20.500.12442/7003 https://doi.org/10.3390/nu12103039 https://www.mdpi.com/2072-6643/12/10/3039 |
dc.language.iso.eng.fl_str_mv |
eng |
language |
eng |
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Attribution-NonCommercial-NoDerivatives 4.0 Internacional |
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Attribution-NonCommercial-NoDerivatives 4.0 Internacional http://creativecommons.org/licenses/by-nc-nd/4.0/ http://purl.org/coar/access_right/c_abf2 |
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MDPI |
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MDPI |
dc.source.eng.fl_str_mv |
Nutrients |
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Vol. 12, No. 10, 2020 |
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Universidad Simón Bolívar |
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Salazar, Juan1be82f2b-2e1c-497f-b8c3-789a462fc4f2Angarita, Lissécd37d36e-0d41-457f-9dc8-1ed5b9201b16Morillo, Valeryf3f6dd3c-b192-4bf7-83c7-b7b1400b56b3Navarro, Carlae0012636-ad49-43ac-b575-384725db4facMartínez, María Sofía0dda0581-5723-45c7-baaa-ff01d6379071Chacín, Maricarmenfdb0f1d1-c963-4360-8d3b-f21d402ee436Torres, Wheeler8bebaba2-fe5b-4212-8990-49506592a59eRajotia, Arush7b711d22-c609-42bf-9f22-785c8079195cRojas, Milagros3283fd88-1355-4c19-9a5a-47a9e268ad27Cano, Clímacob7d55d6b-f1bf-4136-9b90-54a80ab90ab2Añez, Roberto233a8885-3f6a-4c67-ab42-f44cd09e3b3fRojas, Joselyn07d42fd8-6b58-4bbf-96e1-fc1f43eee7dbBermúdez, Valmore41d9bc65-14f2-4c9e-9590-5f977e2d60a92021-01-20T23:07:35Z2021-01-20T23:07:35Z202020726643https://hdl.handle.net/20.500.12442/7003https://doi.org/10.3390/nu12103039https://www.mdpi.com/2072-6643/12/10/3039Diabetes 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.pdfengMDPIAttribution-NonCommercial-NoDerivatives 4.0 Internacionalhttp://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccesshttp://purl.org/coar/access_right/c_abf2NutrientsVol. 12, No. 10, 2020DiabetesInflammationMicrobiotaDysbiosisLipopolysaccharidesShort-chainFatty acidsMicrobiota and Diabetes Mellitus: Role of Lipid Mediatorsinfo:eu-repo/semantics/articleArtículo científicohttp://purl.org/coar/version/c_970fb48d4fbd8a85http://purl.org/coar/resource_type/c_2df8fbb1International Diabetes Federation. IDF Diabetes Atlas. 2015. Available online: https://www.idf.org/elibrary/ epidemiology-research/diabetes-atlas/13-diabetes-atlas-seventh-edition.html (accessed on 20 March 2020).De La Cruz Vargas, J.A.; Dos Santos, F.; Dyzinger, W.; Herzog, S. Medicina Del Estilo de Vida: Trabajando Juntos Para Revertir La Epidemia de Las Enfermedades Crónicas En Latinoamérica. Cienc. Innov. Salud 2017, 4. [CrossRef]Baratieri, T.; Dal Santo Ottoni, J.; Luciana Botti, M.; Serpa Maicel, R.D.C.; Gramazio Soares, L. Risco Cardiovascular Em Usuários de Programa de Atenção a Hipertensos e Diabéticos Em Um Município Do Paraná-Brasil. Cienc. Innov. Salud 2014, 2. [CrossRef]Morales, J.; Carcausto, W.; Varillas, Y.; Pérez, J.; Salsavilca, E.; Castro, I.; Rivera, M.; Quispe, M. Actividad Física En Pacientes Con Diabetes Mellitus Del Primer Nivel de Atención de Lima Norte. Rev. Latinoam. Hipertens. 2018, 13, 49–54Gonzalez, C.M.C.; Quiroz, E.A.N.; Lastre-Amell, G.; Oróstegui-Santander, M.A.; Peña, G.E.G.; Sucerquia, A.; Carrero, L.L.S. Dislipidemia como factor de riesgo cardiovascular: Uso de probióticos en la terapéutica nutricional. Arch. Venez. Farmacol. Ter. 2020, 39, 126–139.Rodríguez Nieves, R.R.; Torres Ruiz, L.E.; Sarmiento Segarra, K.B.; Narea Illescas, D.I.; Araque Pluas, I.V.; Apolo Montero, A.M.; Ibarra Vélez, L.S.; Alvarado Chiquito, O.L. Prevalencia de Síndrome Metabólico En Trabajadores de Una Empresa de Construcción En Guayaquil, Ecuador. Rev. Latinoam. Hipertens. 2019, 14, 638–643.Zozulinska, D.; Wierusz-Wysocka, B. Type 2 Diabetes Mellitus as Inflammatory Disease. Diabetes Res. Clin. Pract. 2006, 74, S12–S16. [CrossRef]Román-Pintos, L.M.; Villegas-Rivera, G.; Rodríguez-Carrizalez, A.D.; Miranda-Díaz, A.G.; Cardona-Muñoz, E.G. Diabetic Polyneuropathy in Type 2 Diabetes Mellitus: Inflammation, Oxidative Stress, and Mitochondrial Function. J. Diabetes Res. 2016, 2016, 3425617. [CrossRef]Romero, G. Influencia de La Microbiota Intestinal En La Enfermedad Hepática Crónica. Su Rol En El Hepatocarcinoma. Gen 2016, 70, 64–69Vargas-Robles, D.D.; Domínguez-Bello, M.G. Microbiota de los indígenas del Amazonas venezolano: Influencia de los estilos de vida. Gac. Med. Caracas 2020, 126, 291–303.Torres, Y.; Bermúdez, V.; Garicano, C.; Vilasmil, N.; Bautista, J.; Martínez, M.S.; Rojas-Quintero, J. Desarrollo del sistema inmunológico ¿naturaleza o crianza? Arch. Venez. Farmacol. Ter. 2017, 36, 144–151.Faneite Antique, D.P.; Faneite Campos, J. Microbioma perinatal: Nuevos horizontes de la vida. Gac. Med. Caracas 2020, 123, 94–106Ruiz, L.; Delgado, S.; Ruas-Madiedo, P.; Sánchez, B.; Margolles, A. Bifidobacteria and Their Molecular Communication with the Immune System. Front. Microbiol. 2017, 8, 2345. [CrossRef]García, P.O. La fibra alimentaria y su uso terapéutico en algunas enfermedades crónicas. Gac. Med. Caracas 2020, 120, 107–114.Dávila, L.A.; Pirela, V.B.; Díaz, W.; Villasmil, N.R.; León, S.C.; Contreras, M.C.E.; Bonacich, K.B.; Agüero, S.D.; Vergara, P.C.; Bonacich, R.B.; et al. The Microbiome and the Epigenetics of Diabetes Mellitus. In Diabetes Food Plan; Waisundara, V., Ed.; InTech: London, UK, 2018.Carpio Duran, A.L.; Duran Medina, M.F.; Andrade Valdivieso, M.R.; Espinoza Dunn, M.A.; Rodas Torres, W.P.; Abad Barrera, L.N.; Rodríguez Barzola, C.V.; Yagual Villon, O.A. Terapia Incretinomimética: Evidencia Clínica de La Eficacia de Los Agonistas Del GLP-1R y Sus Efectos Cardio-Protectores. Rev. Latinoam. Hipertens. 2018, 13, 400–415Dávila, L.A.; Pirela, V.B.; Villasmil, N.R.; Cisternas, S.; Díaz, W.; Escobar, M.C.; Carrasco, P.; Durán, S.; Buhring, K.; Buhring, R.; et al. New Insights into Alleviating Diabetes Mellitus: Role of Gut Microbiota and a Nutrigenomic Approac. In Diabetes Food Plan; Waisundara, V., Ed.; InTech: London, UK, 2018.Bolívar González, S.; Talero Barrientos, E.; Motilva Sánchez, V. Efectos de Un Preparado Probiótico En Un Modelo de Colitis Experimental Crónica En Ratones, Inducida Por La Ingesta de Dextrano Sulfato Sódico (DSS). Cienc. Innov. Salud 2015, 3. 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Available online: http://apps.who.int/iris/bitstream/10665/204871/1/9789241565257_eng.pdf (accessed on 20 March 2020).De Fronzo, R.A. From the Triumvirate to the Ominous Octet: A New Paradigm for the Treatment of Type 2 Diabetes Mellitus. Diabetes 2009, 58, 773–795. [CrossRef] [PubMed]Schwartz, S.S.; Epstein, S.; Corkey, B.E.; Grant, S.F.A.; Gavin, J.R.; Aguilar, R.B. The Time Is Right for a New Classification System for Diabetes: Rationale and Implications of the β-Cell–Centric Classification Schema. Diabetes Care 2016, 39, 179–186. [CrossRefVatanen, T.; Kostic, A.D.; D’Hennezel, E.; Siljander, H.; Franzosa, E.A.; Yassour, M.; Kolde, R.; Vlamakis, H.; Arthur, T.D.; Hämäläinen, A.-M.; et al. Variation in Microbiome LPS Immunogenicity Contributes to Autoimmunity in Humans. Cell 2016, 165, 842–853. [CrossRef]Brown, K.; Godovannyi, A.; Ma, C.; Zhang, Y.; Ahmadi-Vand, Z.; Dai, C.; Gorzelak, M.A.; Chan, Y.; Chan, J.M.; Lochner, A.; et al. 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[CrossRef]Mobini, R.; Tremaroli, V.; Ståhlman, M.; Karlsson, F.; Levin, M.; Ljungberg, M.; Sohlin, M.; Bertéus Forslund, H.; Perkins, R.; Bäckhed, F.; et al. Metabolic Effects of Lactobacillus Reuteri DSM 17938 in People with Type 2 Diabetes: A Randomized Controlled Trial. Diabetes Obes. Metab. 2017, 19, 579–589. [CrossRef] [PubMed]Ahmad, R.; Thomas, R.; Kochumon, S.; Sindhu, S. Increased Adipose Tissue Expression of IL-18R and Its Ligand IL-18 Associates with Inflammation and Insulin Resistance in Obesity. Immun. Inflamm. Dis. 2017, 5, 318–335. [CrossRef]Yan, Y.; Li, S.; Liu, Y.; Bazzano, L.; He, J.; Mi, J.; Chen, W. Temporal Relationship between Inflammation and Insulin Resistance and Their Joint Effect on Hyperglycemia: The Bogalusa Heart Study. Cardiovasc. Diabetol. 2019, 18, 109. [CrossRef]Esser, N.; Legrand-Poels, S.; Piette, J.; Scheen, A.J.; Paquot, N. Inflammation as a Link between Obesity, Metabolic Syndrome and Type 2 Diabetes. Diabetes Res. Clin. Pract. 2014, 105, 141–150. [CrossRef]Roohi, A.; Tabrizi, M.; Abbasi, F.; Ataie-Jafari, A.; Nikbin, B.; Larijani, B.; Qorbani, M.; Meysamie, A.; Asgarian-Omran, H.; Nikmanesh, B.; et al. Serum IL-17, IL-23, and TGF-β Levels in Type 1 and Type 2 Diabetic Patients and Age-Matched Healthy Controls. Biomed. Res. Int. 2014, 2014, 718946. [CrossRef] [PubMed]Abdel-Moneim, A.; Bakery, H.H.; Allam, G. The Potential Pathogenic Role of IL-17/Th17 Cells in Both Type 1 and Type 2 Diabetes Mellitus. Biomed. Pharmacother. 2018, 101, 287–292. [CrossRef] [PubMed]Von Scholten, B.J.; Reinhard, H.; Hansen, T.W.; Schalkwijk, C.G.; Stehouwer, C.; Parving, H.-H.; Jacobsen, P.K.; Rossing, P. Markers of Inflammation and Endothelial Dysfunction Are Associated with Incident Cardiovascular Disease, All-Cause Mortality, and Progression of Coronary Calcification in Type 2 Diabetic Patients with Microalbuminuria. J. Diabetes Complicat. 2016, 30, 248–255. 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