Intestinal microbiota and its relationship to metabolic disorders
Keywords:
Intestinal microbiota, metabolism and inflammation, rodentsAbstract
The complex of organisms that inhabit the intestine and which includes a large number of bacteria, fungi, yeasts, viruses and phage is known as Intestinal Microbiota (MI). The balance between the MI, the epithelial barrier and the local immune system determines intestinal homeostasis in the healthy subject. MI is important in regulating the rescue and energy expenditure, as well as in fat storage and food intake in the host. Due to the increasing impact of metabolic disorders in society, the need to compile, summarize and analyze the most relevant bibliography on recent advances in the understanding of the intestinal microbiota and its possible relationship with these disorders. Investigations with experimental rodent models suggest that the bacterial composition, functional genes and metabolic activities of IM are altered in subjects with obesity, metabolic syndrome or type 2 diabetes (DT2). In addition, it appears that dietary fat is also an important factor affecting the composition of MI, as well as the barrier function of the intestine and therefore, plasma levels of LPS, producing a metabolic endotoxemia that could contribute to the development low-grade systemic inflammation, insulin resistance and DT2. Finally, recent research in rodents indicates that there is a relationship between MI and the pathogenesis of obesity, metabolic syndrome and even DT2.
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2. Qin J, Li R, Raes J, Arumugam M, Burgdorf KS, Manichanh C, et al. A human gut microbial gene cata-logue established by metagenomic sequencing. Nature. 2010; 464:59-65.
3. Kyu Y, y Lee M. Gut Microbiota and Metabolic Disorders. Diabetes Metab J.2015; 39:198-203.
4. Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mar¬dis ER, Gordon JI. An obesity-associated gut microbi¬ome with increased capacity for energy harvest. Nature. 2006; 444:1027-31.
5. Ley RE, Backhed F, Turnbaugh P, Lozupone CA, Knight RD, Gordon JI. Obesity alters gut microbial ecology. Proc Natl Acad Sci USA. 2005; 102:11070-5.
6. Devaraj S, Hemarajata P, Versalovic J. La microbiota intestinal humana y el metabolismo corporal: Implicaciones con la obesidad y la diabetes. Acta Bioquím Clín Latinoam. 2013; 47(2):421-34.
7. Backhed F, Manchester JK, Semenkovich CF, Gordon JI. Mechanisms underlyingthe resistance to diet-in¬duced obesity in germ-free mice. Proc Natl Acad SciUSA. 2007; 104:979-84.
8. Gotteland, M. El papel de la microbiota intestinal en el desarrollo de la obesidad y de la diabetes de tipo-2. Rev Chil Endocrinol Diabetes. 2013; 6(4):155-162.
9. Hildebrandt MA, Hoffmann C, Sherrill-Mix SA, Keilbaugh SA, Hamady M, Chen YY, et al. Highfat diet determines the composition of the murine gut microbiome independently of obesity. Gastroenterology. 2009; 137:1716-24.
10. Cani PD, Delzenne NM. Involvement of the gut micro-biota in the development of low grade inflammation as-sociated with obesity: focus on this neglected partner. Acta Gastroenterol Belg. 2010; 73:267-9.
11. Ley RE. Obesity and the human microbiome. Curr Opin Gastroenterol. 2009; 26:5-11.
12. Ravussin Y, Koren O, Spor A, LeDuc C, Gutman R, Stombaugh J, et al. Responses of gut microbiota to diet composition and weight loss in lean and obese mice. Obesity. 2011; 20:738-47.
13. Dethlefsen L, Relman DA. Incomplete recovery and individualized responses of the human distal gut mi-crobiota to repeated antibiotic perturbation. Proc Natl Acad Sci USA. 2010; 108 Suppl 1:4554-61.
14. Carvalho BM, Guadagnini D, Tsukumo DM, Schenka AA, Latuf-Filho P, Vassallo J, et al. Modulation of gut microbiota by antibiotics improves insulin signallingin high-fat fed mice. Diabetologia.2012; 55:2823-34.
15. Vijay-Kumar M, Aitken JD, Carvalho FA, Cullender TC, Mwangi S. Metabolic syndrome and altered gut microbiota in mice lacking Toll-like receptor 5. Science. 2010; 328:228-31.
16. Frazier TH, DiBaise JK, McClain CJ. Gut microbiota, intestinal permeability, obesity-induced inflammation, and liver injury. JPEN J Parenter Enteral Nutr. 2011; 35 Suppl 5:S14-S20.
17. McNeil NI. The contribution of the large intestine to energy supplies in man. Am J Clin Nutr. 1984; 39:338-42.
18. Brown AJ, Goldsworthy SM, Barnes AA, Eilert MM, Tcheang L. The Orphan G protein-coupled receptors GPR41 and GPR43 are activated by propionate and other short chain carboxylic acid. J Biol Chem. 2003; 278:11312-9.
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