There's an active debate as to whether saturated fats directly activate Toll-like-receptors, or whether this is an artifact of low-level endotoxin contamination of most fatty acid sources.
Erridge, C., & Samani, N. J. (2009). Saturated fatty acids do not directly stimulate Toll-like receptor signaling. Arteriosclerosis, thrombosis, and vascular biology, 29(11), 1944-1949.
Huang, S., Rutkowsky, J. M., Snodgrass, R. G., Ono-Moore, K. D., Schneider, D. A., Newman, J. W., ... & Hwang, D. H. (2012). Saturated fatty acids activate TLR-mediated proinflammatory signaling pathways. Journal of lipid research,53(9), 2002-2013.
What's uncontested at this point is that high saturated fat diets and meals increase plasma endotoxins, both by modulating the gut microbiota and by increasing intestinal permeability. I'll let the titles tell the story:
Erridge, C., Attina, T., Spickett, C. M., & Webb, D. J. (2007). A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation. The American journal of clinical nutrition, 86(5), 1286-1292.
Cani, P. D., Bibiloni, R., Knauf, C., Waget, A., Neyrinck, A. M., Delzenne, N. M., & Burcelin, R. (2008). Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet–induced obesity and diabetes in mice. Diabetes, 57(6), 1470-1481.
Ghoshal, S., Witta, J., Zhong, J., De Villiers, W., & Eckhardt, E. (2009). Chylomicrons promote intestinal absorption of lipopolysaccharides. Journal of lipid research, 50(1), 90-97.
Ghanim, H., Abuaysheh, S., Sia, C. L., Korzeniewski, K., Chaudhuri, A., Fernandez-Real, J. M., & Dandona, P. (2009). 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 implications for insulin resistance. Diabetes care, 32(12), 2281-2287.
Suzuki, T., & Hara, H. (2010). Dietary fat and bile juice, but not obesity, are responsible for the increase in small intestinal permeability induced through the suppression of tight junction protein expression in LETO and OLETF rats. Nutr Metab (Lond), 7(1), 19.
Rabot, S., Membrez, M., Bruneau, A., Gérard, P., Harach, T., Moser, M., ... & Chou, C. J. (2010). Germ-free C57BL/6J mice are resistant to high-fat-diet-induced insulin resistance and have altered cholesterol metabolism. The FASEB Journal, 24(12), 4948-4959.
Laugerette, F., Vors, C., Géloën, A., Chauvin, M. A., Soulage, C., Lambert-Porcheron, S., ... & Michalski, M. C. (2011). Emulsified lipids increase endotoxemia: possible role in early postprandial low-grade inflammation. The Journal of nutritional biochemistry, 22(1), 53-59.
Pendyala, S., Walker, J. M., & Holt, P. R. (2012). A high-fat diet is associated with endotoxemia that originates from the gut. Gastroenterology, 142(5), 1100-1101.
Kim, K. A., Gu, W., Lee, I. A., Joh, E. H., & Kim, D. H. (2012). High fat diet-induced gut microbiota exacerbates inflammation and obesity in mice via the TLR4 signaling pathway. PLoS One, 7(10), e47713.
Clemente-Postigo, M., Queipo-Ortuno, M. I., Murri, M., Boto-Ordonez, M., Perez-Martinez, P., Andres-Lacueva, C., ... & Tinahones, F. J. (2012). Endotoxin increase after fat overload is related to postprandial hypertriglyceridemia in morbidly obese patients. Journal of lipid research, 53(5), 973-978.
Harte, A. L., Varma, M. C., Tripathi, G., McGee, K. C., Al-Daghri, N. M., Al-Attas, O. S., ... & McTernan, P. G. (2012). High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects.Diabetes care, 35(2), 375-382.
Shrestha, U. K. (2012). High-fat diet is associated with endotoxemia and low-grade inflammation. Nepal Journal of Medical Sciences, 1(2), 62-63.
Serino, M., Luche, E., Gres, S., Baylac, A., Bergé, M., Cenac, C., ... & Burcelin, R. (2012). Metabolic adaptation to a high-fat diet is associated with a change in the gut microbiota. Gut, 61(4), 543-553.
Laugerette, F., Furet, J. P., Debard, C., Daira, P., Loizon, E., Géloën, A., ... & Michalski, M. C. (2012). Oil composition of high-fat diet affects metabolic inflammation differently in connection with endotoxin receptors in mice.American Journal of Physiology, 302(3), E374-E386.
Mani, V., Hollis, J. H., & Gabler, N. K. (2013). Dietary oil composition differentially modulates intestinal endotoxin transport and postprandial endotoxemia. Nutr Metab, 10(6).
Zaman, G. S., Zaman, F., & Rasul, M. G. (2014) Comparison of postprandial endotoxemia in male adolescents and male subjects above 50 years after a fat overload.
Reviews:
Moreira, A. P. B., Texeira, T. F. S., Ferreira, A. B., do Carmo Gouveia Peluzio, M., & de Cássia Gonçalves Alfenas, R. (2012). Influence of a high-fat diet on gut microbiota, intestinal permeability and metabolic endotoxaemia. British Journal of Nutrition, 108(05), 801-809.
Herieka, M., & Erridge, C. (2014). High‐fat meal induced postprandial inflammation. Molecular nutrition & food research, 58(1), 136-146.
Shen, W., Gaskins, H. R., & McIntosh, M. K. (2014). Influence of dietary fat on intestinal microbes, inflammation, barrier function and metabolic outcomes. The Journal of nutritional biochemistry, 25(3), 270-280.
High dietary fructose is also implicated in metabolic endotoxemia, through encouraging small intestinal dysbiosis. The whole metabolic endotoxemia story is one of the most interesting, and most underreported, stories from recent nutritional science.
Edited by Darryl, 18 January 2015 - 04:42 PM.