INFLUÊNCIA DA DIETA NA ENDOTOXEMIA METABÓLICA

Autores

  • Ana Paula Boroni Moreira Universidade Federal de Juiz de Fora, Departamento de Nutrição, Juiz de Fora – MG

Resumo

O lipopolissacarídeo (LPS) pode desempenhar um papel importante no desenvolvimento de doenças crônicas, tais como obesidade e diabetes. Essa endotoxina é capaz de se ligar ao Toll-like receptor (TLR-4) presente na membrana plasmática de diferentes tipos celulares, que por sua vez desencadeia diversas vias de sinalização. Essas vias quando ativadas podem acarretar inflamação, induzindo resistência insulínica por meio de distintos mecanismos. A dieta pode desempenhar um papel importante no desenvolvimento da endotoxemia. Entre os fatores dietéticos, a ingestão excessiva de lipídio tem se destacado. Outros compostos, tais como probióticos, prebióticos, flavonoides e frutose também podem influenciar o LPS circulante. Assim, o objetivo desta revisão é integrar o novo conhecimento referente às interações entre nutrientes e endotoxemia metabólica

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Referências

AMAR, J. et al. Energy intake is associated with endotoxemia in apparently health men. American Journal of Clinical Nutrition, Bethesda, v. 87, no. 5, p. 1219–1223, 2008.

BASTOS, D.H.M.; ROGERO, M.M.; ARÊAS, J.A.G. Mecanismos de ação de compostos bioativos dos alimentos no contexto de processos inflamatórios relacionados à obesidade. Arquivos Brasileiros de Endocrinologia & Metabologia, São Paulo, v. 53, no. 5, p. 646-656, 2009.

BASU, S. et al. Pregravid obesity associates with increased maternal endotoxemia and metabolic inflammation. Obesity, Silver Spring, v. 19, no. 3, p. 476-482, 2011.

BERG RD. The indigenous gastrointestinal microflora. Trends in Microbiology, Cambridge, v. 4, no. 11, p. 430–435, 1996.

BRUN, P. et al. Increased intestinal permeability in obese mice: new evidence in the pathogenesis of nonalcoholic steatohepatitis. American Journal of Physiology. Gastrointestinal Liver and Physiology, Bethesda, v. 292, no. 2, p. G518-G525, 2007.

CANI, P.D.; DELZENNE, N.M. The gut microbiome as therapeutic target. Pharmacology & Therapeutics, Oxford, v. 130, no. 2, p. 202–212, 2011.

CANI, P.D. et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes, New York, v. 56, no. 7, p. 1761-1772, 2007a.

CANI, P.D. et al. Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia. Diabetologia, Berlin, v. 50, no. 11, p. 2374–2383, 2007b.

CANI, P.D. et al. Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fatdiet-induced obesity and diabetes in mice. Diabetes, New York, v. 57, no. 6, p. 1470–1481, 2008.

CLEMENTE-POSTIGO, M. et al. Endotoxin increase after fat overload is related to postprandial hypertriacylglycerolmia in morbidly obese patients. Journal of Lipid Research, Memphis, v. 53, no. 5, p. 973-978, 2012.

CORDAIN, L. et al. Origins and evolution of the Western diet: health implications for the 21st century. American Journal of Clinical Nutrition, Bethesda, v. 81, no. 2, p. 341–354, 2005.

CREELY, S.J. et al. Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes. American Journal of Physiology. Endocrinology and Metabolism, Bethesda, v. 292, no. 3, p. E740–E747, 2007.

DE BANDT, J.P.; WALIGORA-DUPRIET, A.J.; BUTEL, M.J. Intestinal microbiota in inflammation and insulin resistance: relevance to humans. Current Opinion in Clinical Nutrition and Metabolic Care, London, v. 14, no. 4, p. 334–340, 2011.

DEFRONZO, R.A. Insulin resistance, lipotoxicity, type 2 diabetes and atherosclerosis: the missing links. The Claude Bernard Lecture 2009. Diabetologia, Berlin, v. 53, no. 7, p. 1270–1287, 2010.

DELZENNE, N.M.; CANI, P.D. Gut microbiota and the pathogenesis of insulin resistance. Current Diabetes Report, Philadelphia, v. 11, no. 3, p. 154–159, 2011.

DEOPURKAR, R. et al. Differential effects of cream, glucose and orange juice on inflammation, endotoxin, and the expression of toll-like receptor-4 and suppressor of cytokine signaling-3. Diabetes Care, New York, v. 33, no. 5, p. 991–997, 2010.

DING, S.; LUND, P.K. Role of intestinal inflammation as an early event in obesity and insulin resistance. Current Opinion in Clinical Nutrition and Metabolic Care, London, v. 14, no. 4, p 328–33, 2011.

ERRIDGE, C. et al. A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial in flammation. American Journal of Clinical Nutrition, Bethesda, v. 86, no. 5, p. 1286 – 1292, 2007.

GERALDO, J.M.; ALFENAS, R.C.G. Papel da dieta na prevenção e no controle da inflamação crônica – evidências atuais. Arquivos Brasileiros de Endocrinologia & Metabologia, São Paulo, v. 52, no. 6, p. 951-967, 2008.

GHANIM, H. et al. Increase in plasma endotoxin concentrations and the expression of toll-like receptors and suppressor of cytokine signaling-3 in mononuclear cells after a high-fat, high-carbohydrate meal. Diabetes Care, New York, v. 32, no. 12, p. 2281–2287, 2009.

GHANIM, H. et al. Orange juice neutralizes the proinflammatory effect of a high-fat, high-carbohydrate meal and prevents endotoxin increase and toll-like receptor expression. American Journal of Clinical Nutrition, Bethesda, v. 91, no. 4, p. 940–949, 2010.

GHOSHAL, S. et al. Chylomicrons promote intestinal absorption of lipopolysaccharides. Journal of Lipid Reserach, Memphis, v. 50, no. 1, p. 90–97, 2009.

GRIMALDI, E. et al. Proinflammatory signal transduction pathway induced by shigella flexneri porins in caco-2 cells. Brazilian Journal of Microbiology, São Paulo, v. 40, n. 3, p. 701-709, 2009.

HARTE, A.L. et al. High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects. Diabetes Care, New York, v. 35, no. 2, p. 375-382, 2012.

HATTORI, M.; TAYLOR, T.D. The human intestinal microbiome: a new frontier of human biology. DNA Research, Tokyo, v. 16, no. 1, p. 1-12, 2009.

KAVANAGH, K. et al. Dietary fructose induces endotoxemia and hepatic injury in calorically controlled primates. American Journal of Clinical Nutrition, Bethesda, v. 98, no. 2, p. 349-357, 2013.

LAPARRA, J.M.; SANZ, Y. Interactions of gut microbiota with functional food components and nutraceuticals. Pharmacological Research, London, v. 61, no. 3, p. 219–225, 2010.

LAUGERETTE, F.C. et al. Emulsified lipids increase endotoxemia: possible role in early postprandial low-grade inflammation. The Journal of Nutritional Biochemistry, Stoneham, v. 22, no. 1, p. 53-59, 2011a.

LAUGERETTE, F. et al. Complex links between dietary lipids, endogenous endotoxins and metabolic inflammation. Biochimie, Paris, v. 93, no. 1, p. 39-45, 2011b.

LAUGERETTE, F. et al. Overfeeding increases postprandial endotoxemia in men: Inflammatory outcome may depend on LPS transporters LBP and sCD14. Molecular Nutrition & Food Reserach, Weinheim, p. 1–6, 2014.

MANCO, M.; PUTIGNANI, L.; BOTTAZZO, G.F. Gut microbiota, lipopolysaccharides, and innate immunity in the pathogenesis of obesity and cardiovascular risk. Endocrine Reviews, Baltimore, v. 31, no. 6, p.817-844, 2010.

MUSSO, G.; GAMBINO, R.; CASSADER, M. Obesity, Diabetes, and Gut Microbiota. The hygiene hypothesis expanded? Diabetes Care, New York, v. 33, no. 10, p. 2277-2284, 2010.

O'CONNOR, E.M.; O'HERLIHY, E.A.; O'TOOLE, P.W. Gut microbiota in older subjects: variation, health consequences and dietary intervention prospects. The Proceedings of the Nutrition Society, London, v. 13, p. 1-11, 2014.

PAN, Z.K. Toll-like receptors and TLR-mediated signaling: more questions than answers. American Journal of Physiology. Lung Cellular and Molecular Physiology, Bethesda, v. 286, no. 5, p. L918-L920, 2004.

PHILLIPS, M.L. Gut reaction: environmental effects on the human microbiota. Environmental Health Perspectives, v. 117, no. 5, p. A198-A205, 2009.

PUSSINEN, P.J. et al. Endotoxemia is associated with an increased risk of incident diabetes. Diabetes Care, New York, v. 34, no. 2, p. 392-397, 2011.

QIN, J. et al. A human gut microbial gene catalogue established by metagenomic sequencing. Nature. London, v. 464, no. 7285, p. 59-65, 2010.

RAETZ, C.R.H.; WHITFIELD, C. Lipopolysaccharide Endotoxins. Annual Review of Biochemistry, Palo Alto, v. 71, p. 635–700, 2002.

SHANIK, M.H. et al. Insulin resistance and hyperinsulinemia: is hyperinsulinemia the cart or the horse? Diabetes Care, New York, v. 31, no. 2, p. S262-S268, 2008.

SONG, M.J. et al. Activation of Toll-like receptor 4 is associated with insulin resistance in adipocytes. Biochemical and Biophysical Research Communications, New York, v. 346, no. 3, p. 739–745, 2006.

SPRUSS, A. et al. Toll-like receptor 4 is involved in the development of fructose-induced hepatic steatosis in mice. Hepatology, Baltimore, v. 50, no. 4, p. 1094–1104, 2009.

SUZUKI, T.; HARA, H. Dietary fat and bile juice, but not obesity, are responsible for the increase in small intestinal permeability induced through the suppression of tight High-fat diet and endotoxemia junction protein expression in LETO and OLETF rats. Nutrition & Metabolism, London, v. 7, p. 19, 2010.

TUIN, A. et al. On the role and fate of LPS-dephosphorylating activity in the rat liver. American Journal of Physiology. Gastrointestinal and Liver Physiology, Bethesda, v. 290, no. 2, p. G377-G385, 2006.

USAMI, M. et al. Effect of eicosapentaenoic acid (EPA) on tight junction permeability in intestinal monolayer cells. Clinical Nutrition, Edinburgh, v. 20, no. 4, p. 351–335, 2001.

XIN, J. et al. Preventing non-alcoholic fatty liver disease through Lactobacillus johnsonii BS15 by attenuating inflammation and mitochondrial injury and improving gut environment in obese mice. Applied Microbiology and Biotechnology, Berlin, 2014.

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Publicado

2015-08-20

Como Citar

1.
Moreira APB. INFLUÊNCIA DA DIETA NA ENDOTOXEMIA METABÓLICA. HU Rev [Internet]. 20º de agosto de 2015 [citado 21º de novembro de 2024];40(3 e 4). Disponível em: https://periodicos.ufjf.br/index.php/hurevista/article/view/2443

Edição

v. 40 n. 3 e 4 (2014)

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Artigos de Revisão da Literatura

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