Peater Piper
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Generally it's stated that saturated and medium-chain triglycerides improve intestinal barrier function. A frequent example is the protection against ethanol consumption.
Dietary saturated fat reduces alcoholic hepatotoxicity in rats by altering fatty acid metabolism and membrane composition. - PubMed - NCBI
"As dietary saturated fat content increased, all measures of hepatic pathology and oxidative stress were progressively reduced, including steatosis (P < 0.05). Thus, saturated fat protected rats from alcoholic liver disease in a dose-responsive fashion."
The Type of Dietary Fat Modulates Intestinal Tight Junction Integrity, Gut Permeability, and Hepatic Toll-Like Receptor Expression in a Mouse Model of Alcoholic Liver Disease
"After 8 weeks of EtOH feeding liver injury and steatosis were observed in USF+EtOH group compared to control and SF+EtOH. Significantly increased intestinal permeability in conjunction with elevated blood endotoxin levels were observed in the ileal segments of the mice fed USF+EtOH. USF diet alone resulted in down-regulation of intestinal TJ protein mRNA expression compared to SF. Importantly, alcohol further suppressed TJ proteins in USF+EtOH but did not affect intestinal TJ in SF+EtOH group. The type of fat in the diet alone did not affect hepatic TLR expression. Compared to control animals, hepatic TLR (TLR 1, 2, 3, 4, 7, 8, 9) mRNA expression was significantly (p<0.05) increased in USF+EtOH, but not in SF+EtOH group. Notably, TLR5 was the only up-regulated TLR in both SF+EtOH and USF+EtOH groups."
Yet there's a number of studies showing that saturated fats, and especially medium-chain triglycerides increase permeability and absorption to various substances, including endotoxin, at least short-term. How are they protective long-term when they perform so poorly in the short-term?
Absorption enhancement through intracellular regulation of tight junction permeability by medium chain fatty acids in Caco-2 cells. - PubMed - NCBI
"In this study, the absorption-enhancing effects of the sodium salts of two MCFAs, capric acid (C10) and lauric acid (C12), were studied in monolayers of human intestinal epithelial Caco-2 cells. Both MCFAs induced a rapid increase in epithelial permeability to the hydrophilic marker molecule sodium fluorescein. Inhibition of phospholipase C and inhibition or activation of various kinases and buffering of intracellular calcium indicated that the effects on epithelial permeability were mediated through phospholipase C-dependent inositol triphosphate/diacylglycerol pathways."
Nutrition & Metabolism
"Postprandial serum endotoxin concentrations were increased after a meal rich in saturated fatty acids and decreased with higher n-3 PUFA intake. Compared to the no oil control, fish oil and CLO which are rich in n-3 fatty acids reduced ex vivo endotoxin Papp by 50% (P < 0.05). Contrarily, saturated fatty acids increased the Papp by 60% (P = 0.008). Olive and vegetable oils did not alter intestinal endotoxin Papp."
http://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=3795&context=etd
"To assess the effect of dietary lipids on postprandial serum endotoxin concentrations, pigs received a porridge meal containing either 50 mL of saline, CO, VO or FO. The endotoxin concentration of the various oils used did not differ (data not shown). Change in postprandial serum endotoxin concentration due to different meal treatments are presented in Figure 1A. The overall postprandial serum endotoxin concentrations were significantly lower in the meals constituting saline or FO, with the mean overall serum endotoxin concentration 71 increasing two-fold over the saturated coconut oil meal treatment (P<0.05, Figure 1B). However, meals made up with VO were not different from the saline, CO or FO treatments (P<0.05). Interestingly, the CO meal significantly elevated serum endotoxin concentrations after 2 hours versus the saline and FO, and these remained elevated at 3 and 5 hour postprandial (P<0.05, Figure 1A)."
From the above paper, they also go on to hypothesize that high fiber diets increase gram positive bacteria, while diets high in saturated fat increase gram negative bacteria (endotoxin), although milk fat doesn't seem to have the same affect.
"Gram negative bacteria, particularly those found in the distal ileum and colon might be one of the major sources for circulating endotoxin [33]. It has been estimated that a single cell of Escherichia coli contains approximately 106 Lipid A or endotoxin molecules and a typical human intestinal tract could harbor approximately one gram of endotoxin [33-35]. Interestingly, the bacterial population in the intestine is not static. Multiple studies have shown that bacterial composition shifts to either gram positive majority or gram negative majority based on the composition of the diet consumed [36-38]. A majority of these studies show that consuming high saturated fat diet for longer period results in higher gram negative bacterial populations and high fiber diets results in gram positive bacterial populations. Even though there are no known techniques available to identify which bacterial species the LPS molecules originated from, it is believed that this endotoxemia is due to a raise in Enterobacteriaceae [37, 39]. Laugerette et al. [6], reaffirmed this and showed that fatty acid composition of different dietary oils can alter intestinal microbiota populations. Moreover, these authors demonstrated that feeding a diet high in palm oil which is rich in SFAs significantly increased the gram negative bacteria Escherichia coli groups, which can be significant source of endotoxin in the cecal content of mice compared to milk fat, rape seed and sunflower oil fed diets."
Dietary saturated fat reduces alcoholic hepatotoxicity in rats by altering fatty acid metabolism and membrane composition. - PubMed - NCBI
"As dietary saturated fat content increased, all measures of hepatic pathology and oxidative stress were progressively reduced, including steatosis (P < 0.05). Thus, saturated fat protected rats from alcoholic liver disease in a dose-responsive fashion."
The Type of Dietary Fat Modulates Intestinal Tight Junction Integrity, Gut Permeability, and Hepatic Toll-Like Receptor Expression in a Mouse Model of Alcoholic Liver Disease
"After 8 weeks of EtOH feeding liver injury and steatosis were observed in USF+EtOH group compared to control and SF+EtOH. Significantly increased intestinal permeability in conjunction with elevated blood endotoxin levels were observed in the ileal segments of the mice fed USF+EtOH. USF diet alone resulted in down-regulation of intestinal TJ protein mRNA expression compared to SF. Importantly, alcohol further suppressed TJ proteins in USF+EtOH but did not affect intestinal TJ in SF+EtOH group. The type of fat in the diet alone did not affect hepatic TLR expression. Compared to control animals, hepatic TLR (TLR 1, 2, 3, 4, 7, 8, 9) mRNA expression was significantly (p<0.05) increased in USF+EtOH, but not in SF+EtOH group. Notably, TLR5 was the only up-regulated TLR in both SF+EtOH and USF+EtOH groups."
Yet there's a number of studies showing that saturated fats, and especially medium-chain triglycerides increase permeability and absorption to various substances, including endotoxin, at least short-term. How are they protective long-term when they perform so poorly in the short-term?
Absorption enhancement through intracellular regulation of tight junction permeability by medium chain fatty acids in Caco-2 cells. - PubMed - NCBI
"In this study, the absorption-enhancing effects of the sodium salts of two MCFAs, capric acid (C10) and lauric acid (C12), were studied in monolayers of human intestinal epithelial Caco-2 cells. Both MCFAs induced a rapid increase in epithelial permeability to the hydrophilic marker molecule sodium fluorescein. Inhibition of phospholipase C and inhibition or activation of various kinases and buffering of intracellular calcium indicated that the effects on epithelial permeability were mediated through phospholipase C-dependent inositol triphosphate/diacylglycerol pathways."
Nutrition & Metabolism
"Postprandial serum endotoxin concentrations were increased after a meal rich in saturated fatty acids and decreased with higher n-3 PUFA intake. Compared to the no oil control, fish oil and CLO which are rich in n-3 fatty acids reduced ex vivo endotoxin Papp by 50% (P < 0.05). Contrarily, saturated fatty acids increased the Papp by 60% (P = 0.008). Olive and vegetable oils did not alter intestinal endotoxin Papp."
http://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=3795&context=etd
"To assess the effect of dietary lipids on postprandial serum endotoxin concentrations, pigs received a porridge meal containing either 50 mL of saline, CO, VO or FO. The endotoxin concentration of the various oils used did not differ (data not shown). Change in postprandial serum endotoxin concentration due to different meal treatments are presented in Figure 1A. The overall postprandial serum endotoxin concentrations were significantly lower in the meals constituting saline or FO, with the mean overall serum endotoxin concentration 71 increasing two-fold over the saturated coconut oil meal treatment (P<0.05, Figure 1B). However, meals made up with VO were not different from the saline, CO or FO treatments (P<0.05). Interestingly, the CO meal significantly elevated serum endotoxin concentrations after 2 hours versus the saline and FO, and these remained elevated at 3 and 5 hour postprandial (P<0.05, Figure 1A)."
From the above paper, they also go on to hypothesize that high fiber diets increase gram positive bacteria, while diets high in saturated fat increase gram negative bacteria (endotoxin), although milk fat doesn't seem to have the same affect.
"Gram negative bacteria, particularly those found in the distal ileum and colon might be one of the major sources for circulating endotoxin [33]. It has been estimated that a single cell of Escherichia coli contains approximately 106 Lipid A or endotoxin molecules and a typical human intestinal tract could harbor approximately one gram of endotoxin [33-35]. Interestingly, the bacterial population in the intestine is not static. Multiple studies have shown that bacterial composition shifts to either gram positive majority or gram negative majority based on the composition of the diet consumed [36-38]. A majority of these studies show that consuming high saturated fat diet for longer period results in higher gram negative bacterial populations and high fiber diets results in gram positive bacterial populations. Even though there are no known techniques available to identify which bacterial species the LPS molecules originated from, it is believed that this endotoxemia is due to a raise in Enterobacteriaceae [37, 39]. Laugerette et al. [6], reaffirmed this and showed that fatty acid composition of different dietary oils can alter intestinal microbiota populations. Moreover, these authors demonstrated that feeding a diet high in palm oil which is rich in SFAs significantly increased the gram negative bacteria Escherichia coli groups, which can be significant source of endotoxin in the cecal content of mice compared to milk fat, rape seed and sunflower oil fed diets."
