Highly saturated fat diet increases endotoxemia

Von Natur.wiki Autoren-Team

Bezug Lopez-Moreno J, Garcia-Carpintero S, Jimenez-Lucina R, et al. Die Wirkung von Nahrungslipiden auf Endotoxämie beeinflusst die postprandiale Entzündungsreaktion. J Agric FoodChem. 2017;65(35):7756-7763. Zielsetzung Es sollte festgestellt werden, ob die langfristige Einnahme von Diäten, die sich in Menge und Qualität von Fett unterscheiden, die postprandiale intestinale Endotoxin-Resorption beeinflusst. Diese Absorption kann für die postprandiale Entzündungsreaktion nach einer fettreichen Mahlzeit verantwortlich sein. Entwurf Randomisierte diätetische Interventionsstudie Teilnehmer Diese Studie wurde im Rahmen der von der Europäischen Union geförderten LIPGENE-Studie durchgeführt. Insgesamt 75 Teilnehmer, bei denen ein metabolisches Syndrom diagnostiziert wurde, schlossen diese Studie ab. Intervention Die Teilnehmer wurden randomisiert und erhielten …
Cover Lopez-Moreno J, Garcia-Carpintero S, Jimenez-Lucina R, et al. The effect of food lipids on endotoxemia influences postprandial inflammatory reaction. J Agric Foodchem. 2017; 65 (35): 7756-7763. Objective It should be determined whether the long-term intake of diets that differ in the amount and quality of fat influences postprandial intestinal endotoxin absorption. This absorption can be responsible for postprandial inflammatory reaction after a high -fat meal. Draft randomized dietary intervention study participant This study was carried out as part of the Lipgene study funded by the European Union. A total of 75 participants, in whom a metabolic syndrome was diagnosed, completed this study. Intervention The participants were randomized and received ... (Symbolbild/natur.wiki)

reference

Lopez-Moreno J, Garcia-Carpintero S, Jimenez-Lucina R, et al. The effect of food lipids on endotoxemia influences postprandial inflammatory reaction. j agric foodchem . 2017; 65 (35): 7756-7763.

objective

It should be determined whether the long-term intake of diets that differ in the amount and quality of fat influences postprandial intestinal endotoxin absorption. This absorption can be responsible for postprandial inflammatory reaction after a high -fat meal.

draft

randomized dietary intervention study

participant

This study was carried out as part of the Lipgenene study funded by the European Union. A total of 75 participants, in whom a metabolic syndrome was diagnosed, completed this study.

Intervention

The participants were randomized and received 1 of 4 isoenergetic diets for 12 weeks. Two of the diets provided 38 % energy from fat: the diet with highly saturated fatty acids (HSFA) and the diet with many simply unsaturated fatty acids (HMUFA). The remaining 2 were low-fat, highly complex carbohydrates (LFHCC) diets and provided 28 % of energy as fat. One of these diets (LFHCC N-3) was supplemented with 1.24 g/d (n-3) pufa.

After 12 weeks with the assigned diet, the participants received a fat request in which they received 0.7 g/kg body weight of the same fat composition that was consumed during the dietary intervention phase.

Primary result measurements

The researchers pursued plasma lipoproteins, glucose and gene expression in peripheral mononuclear blood cells (PBMCs) and adipose tissue. The plasma levels of lipopolysaccharides (LPS) and LPS-binding protein (LBP) were determined soberly and postprandial (4 hours after a fat provocation).

important knowledge

There was a postprandial increase in LPS mirrors among participants who received the HSFA fat challenge (after eating the HSFA diet), but no postprandial changes were found in the 3 other groups. In addition, there was a positive relationship between the LPS mirrors and the gene expression of IKBA and MIF1 in PMCs. The LPS sober mirrors differed between none of the diet groups after the 12-week intervention.

These results suggest that the consumption of the HSFA diet increases the intestinal absorption of LPS, which increases postprandial endotoxemic levels and postprandial inflammation reaction.

practice implications

This study agrees with other studies that show that a meal with a high content of saturated fatty acids increases the LPS transport from the intestine into the serum. Interestingly, there were only significant differences between the groups after the fat burden, since the sober mirrors from LPS do not differ in any of the groups after the 12-week intervention.

This study is part of a growing number of studies that examine LPS production and transport to the serum as a mechanism that triggers nutritional inflammatory reactions.

The shift of intestinal bacterial populations can be the key to relocating "food reactions" and to change a possibly long list of inflammatory states.

lipopolysaccharide is the main component of the outer membranes of gram -knit bacteria. It induces a strong immune response in animals and is therefore often used by researchers to create animal models for asthma, rheumatoid arthritis and other immune diseases. Lipopolysaccharide, a heat-stable bacterial poison, was the first described endotoxin and is responsible for the consequences of certain infectious diseases. 1 It binds to receptors in many cell types, but has a special affinity for monocytes, dendritic cells, macrophages and B cells. Lipopolysaccharide triggers the secretion of inflammatory cytokines, creates superoxides and acts as a pyrogen that causes fever. 2

The formation of LPs by the intestinal bin is now an important factor in many inflammatory diseases, including autoimmunity, allergies, metabolic syndrome, obesity, diabetes, Alzheimer's and a rapidly growing list of other diseases. 3-7 The sudden postprandial increase of uncomfortable and uncomfortable, which some patients feel by eating Formation of LPs by intestinal bacteria or, as this study suggests, caused by an increased absorption of LPS, which is triggered by eating a meal with a high content of saturated fats.

Endotoxin and the subsequent endotoxemia from the intestine are also considered the main predisposure factors for diseases such as arteriosclerosis, sepsis, obesity and diabetes. It was shown that postprandial endotoxemia in particular increases.

In 2013, Mani et al. showed that on saturated fatty acids (coconut oil) meals increased the postprandial endotoxin concentrations in pigs, while meals with high omega-3-pufa fish oil lowered the endotoxin centers. Olive oil and other vegetable oils had no influence. Nevertheless, this knowledge should warn us about the use of coconut oil and other saturated fats in patients, from whom we suspect that they suffer from endotoxemia.

In recent years, the intestinal microbioma has been regarded as a participant in the pathogenesis of obesity and type 2 Diabetes mellitus. Therefore, manipulating the human intestinal microbiota could soon become a therapeutic point of attack for diabetes. 9 It seems that the LPS production is the mediator that increases the intestinal permeability and can trigger this disease. With type 2 diabetes, LPS triggers a milder "hypo-sponsive" immune response, and this could be the reason why diabetics are susceptible to infections and have such difficulties to combat them.

Brian Mcfarlin et al. reported in August 2017 that supplementation with a combined probiotic was useful to reduce endotoxemic postprandial reactions. The participants of his study (n = 75) were scattered and selected on strong endotoxemic postprandial reactions, at least a 5-time postprandial LPS increase compared to their preprender level. The participants were randomized and received either a rice flour placebo or a combination of spore-forming probiotics ( bacillus indicus [hu36], b subtilis [hu58], b-koagulane , b. Licheniformis and b clausii ) for 30 days. The use of the probiotics was connected to a significant reduction in endotoxins by 42 % and a reduction in the triglycerides 24 %. 11 The placebo was connected with a significant increase in endotoxin levels by 36 %, which prompted this reader to have the safety of uncupable rice flour and its effects on the DARMBIOM surprise.

A number of other studies, in vitro and on mice, suggest that various other probiotics can also be useful to reduce LPS-induced inflammatory reactions, at least partially by maintaining intestinal degrees.

The growing base of knowledge about LPS should cause us to rethink some of our previous assumptions. Food -related reactions, which we thought were allergic, could actually be secondary to endotoxin production or an increased absorption by highly saturated fat meals. The "Candida dusting reactions", which some people attribute to the consumption of coconut oil, can actually be an increased endotoxin recording. The displacement of the intestinal bacterial populations can be the key to postponing "food reactions" and to change a potentially long list of inflammatory states.

  1. p. Hitchcock, L. Leive, H. Makela, et. Rietschel, W. Strittmatter, DC Morrison. Lipopolysaccharide nomenclature-past, present and future. J Bacteriol . 1986; 166 (3): 699-705.
  2. Ramana KV, Fadl AA, Tammali R, Reddy AB, Chopra AK, Srivastava SK. The lipopolysaccharide-induced release of inflammatory mediators in RAW264.7 mouse macrophages conveys aldosereductase. jbiolchem ​​. 2006; 281 (44): 33019-33029.
  3. feehley T., Belda-ferre P., Nagler Cr. What does LPS have to do with it? A role for intestinal LPS variants when driving on autoimmune and allergic diseases. Zellwirt microbe . 2016; 19 (5): 572-574.
  4. Munford rs. Detection of gram -negative bacterial lipopolysaccharides: a determinant human diseases? immune infect . 2008; 76 (2): 454-465.
  5. Hersooug LG, Møller P, Loft S. Rolle of lipopolysaccharides from microbiota in fat tissue infections, adipocyte size and pyroptosis in obesity. nutr res rev . 2018: 1-11.
  6. Harsch ia, Konturek PC. The role of the intestinal microbiota in obesity and diabetes mellitus type 2 and type 1: new insights into "old" diseases. med sci (Basel) . 2018; 6 (2). PII: E32.
  7. Wang LM, Wu Q, Kirk Ra, et al. Lipopolysaccharide endoxemia induces the formation of amyloid β and P-Tau in the rat brain. am j nucl med mol imaging . 2018; 8 (2): 86-99.
  8. Mani V, Hollis JH, Gabler NK. The food composition modulates the intestinal endoxine transport and postprandial endotoxemia. Nutr Metab (London) . 2013; 10 (1): 6.
  9. Sato J, Kanazawa A, Watada H. Type-2-Diabetes and Bacteriemia. ann nutr meta b. 2017; 71 (supplement 1): 17-22.
  10. Khondkaryan L, Margaryan S, Poghosyan D, Manukyan G. affected inflammatory reaction to LPS in type 2 diabetes mellitus. intj inflammation . 2018; 2018: 2157434.
  11. Mcfarlin BK, Henning Al, Bowman Em, Gary Ma, Carbajal KM. The oral probiotic nutritional supplement based on spore was associated with a reduced incidence of postprandial endotoxin, triglycerides and disease risk biomarkers. world J Gastrointest pathophysiol . 2017; 8 (3): 117-126.
  12. y. Cui, L. Liu, X. Dou et al. Lactobacillus Reuteri ZJ617 receives the intestinal degrees through the regulation of Tight Junction, Autophagia and Apoptosis in mice that were challenged with lipopolysaccharide. oncotarget . 2017; 8 (44): 77489-77499.