Oral administration of heat-killed Lactobacillus brevis SBC8803 ameliorates alcoholic liver disease in ethanol-containing diet-fed C57BL/6N mice

Segawa, Shuichi; Wakita, Yoshihisa; Hirata, Hiroshi; Watari, Junji

doi:10.1016/j.ijfoodmicro.2008.09.023

Cited by 102 publications

(67 citation statements)

References 35 publications

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“…Although it was not the focus of our follow-up studies, we would highlight that the literature regarding alcohol's effect on the function of PPAR ␣ is also equivocal. While it has been reported that alcohol decreases hepatic expression of PPAR ␣ ( 31, 32 ), others have reported no change or increased PPAR ␣ expression in response to chronic alcohol consumption (33)(34)(35).…”

Section: Discussionmentioning

confidence: 96%

CD36-deficient mice are resistant to alcohol- and high-carbohydrate-induced hepatic steatosis

Clugston

Yuen

et al. 2014

Journal of Lipid Research

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liver failure ( 2 ). As a fi rst stage in the ALD spectrum, alcoholic steatosis has been extensively studied in humans and animal models to better understand the mechanisms leading to fat accumulation in the alcohol-exposed liver. This research has indicated that alcohol has many effects on hepatic lipid metabolism, including dysregulation of pathways associated with fatty acid (FA) synthesis, uptake, and oxidation, and triglyceride (TG) synthesis and export; however, the mechanisms underpinning these changes and their relative importance are only beginning to be understood ( 3 ).CD36 (also known as fatty acid translocase) is a class B scavenger receptor that is expressed on the cell surface and can recognize multiple ligands, including long-chain fatty acids, oxidized lipids, and lipoproteins ( 4 ). CD36 has multiple cell type-specifi c physiological functions; for example, its expression in microvascular endothelial cells is associated with angiogenesis, and in the apical cells of taste buds, it is associated with the detection of dietary fatty acids ( 4, 5 ). CD36 is also a mediator of free fatty acid (FFA) uptake into tissues, particularly adipose, heart, and skeletal muscle ( 6, 7 ). It is thought that CD36 does not normally play a signifi cant role in hepatic FFA uptake; however, under nonphysiological conditions, CD36 is induced in the liver and may contribute to hepatic steatosis ( 6 ). For example, pharmacologic activation of liver X receptors increases CD36 expression and TG accumulation in the liver ( 8 ), adenoviral-mediated overexpression of hepatic CD36 increases FFA uptake and TG accumulation ( 9 ), and liver tissues obtained from patients with nonalcoholic fatty liver disease also have significantly elevated CD36 expression ( 10 ).Our group and others have observed increased hepatic CD36 expression in alcohol-fed mice at the gene and protein levels ( 11-13 ). Given the role of CD36 in facilitating FFA uptake into tissues and the observation that it is upregulated in the alcohol-exposed liver, we hypothesized that CD36 is Abstract CD36 is a scavenger receptor with multiple ligands and cellular functions, including facilitating cellular uptake of free fatty acids (FFAs). Chronic alcohol consumption increases hepatic CD36 expression, leading to the hypothesis that this promotes uptake of circulating FFAs, which then serve as a substrate for triglyceride (TG) synthesis and the development of alcoholic steatosis. We investigated this hypothesis in alcohol-fed wild-type and Cd36 -defi cient ( Cd36 ؊ / ؊ ) mice using low-fat/high-carbohydrate Lieber-DeCarli liquid diets, positing that Cd36 ؊ / ؊ mice would be resistant to alcoholic steatosis. Our data show that the livers of Cd36 ؊ / ؊ mice are resistant to the lipogenic effect of consuming highcarbohydrate liquid diets. These mice also do not further develop alcoholic steatosis when chronically fed alcohol. Surprisingly, we did not detect an effect of alcohol or CD36 deficiency on hepatic FFA uptake; however, the lower baseline levels of hepatic TG in ...

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Section: Discussionmentioning

confidence: 96%

CD36-deficient mice are resistant to alcohol- and high-carbohydrate-induced hepatic steatosis

Clugston

Yuen

et al. 2014

Journal of Lipid Research

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“…This improvement has been found to be associated with reduced markers of intestinal and liver oxidative stress, inflammation and preserved gut barrier function. Orally administered heat-killed Lactobacillus brevis SBC8803 has ameliorated ethanol-induced liver injury and fatty liver, suppressed the overexpression of TNF-α, sterol regulatory element-binding protein (SREBP)-1 and SREBP-2 mRNA in the liver, and upregulated the expression of heat shock protein 25 mRNA in the small intestine (22). Authors have speculated that the inhibition of TNF-α and SREBPs upregulation by L. brevis is due to the inhibition of gut-derived endotoxin migration into the liver through the enhancement of intestinal barrier function by the induction of cytoprotective heat shock proteins (22).…”

Section: Discussionmentioning

confidence: 99%

“…Orally administered heat-killed Lactobacillus brevis SBC8803 has ameliorated ethanol-induced liver injury and fatty liver, suppressed the overexpression of TNF-α, sterol regulatory element-binding protein (SREBP)-1 and SREBP-2 mRNA in the liver, and upregulated the expression of heat shock protein 25 mRNA in the small intestine (22). Authors have speculated that the inhibition of TNF-α and SREBPs upregulation by L. brevis is due to the inhibition of gut-derived endotoxin migration into the liver through the enhancement of intestinal barrier function by the induction of cytoprotective heat shock proteins (22). In mice treated with MCDD, TNF-α protein levels have been reported to increase by 2.2-fold in the liver compared with mice fed the control diet (50).…”

Section: Discussionmentioning

confidence: 99%

“…Treatment with oral probiotic VSL#3, consisting of eight probiotic strains, has been reported to significantly improve the high fat diet-induced hepatic NKT cell depletion, insulin resistance and hepatic steatosis (21). In another study, Lactobacillus GG (16) and heat-killed Lactobacillus brevis SBC8803 (22) have been shown to ameliorate ethanol-induced liver injury and fatty liver. In contrast, VSL#3 has failed to prevent methionine choline-deficient diet (MCDD)-induced liver steatosis or inflammation, but to ameliorate MCDD-induced liver fibrosis (23).…”

Section: Introductionmentioning

confidence: 99%

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Effects of probiotics on methionine cholinedeficient diet-induced steatohepatitis in rats

Karahan

Işler²,

Koyu³

et al. 2012

Turk J Gastroenterol

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Amaç: ‹ntestinal bakteriler, hepatik insülin direnci ve non-alkolik ya¤l› karaci¤er hastal›¤›nda patojenik rol oynayan endojen sinyalleri indük-lerler. Probiyotikler barsak floras›n› düzenleyerek karaci¤er-barsak ekseninde etki gösterebilirler. Bu çal›flmada s›çan modellerinde metiyonin ve kolinden fakir diyet ile oluflturulan non-alkolik steatohepatitte iki probiyotik kar›fl›m›n›n

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“…We identified these GABA-producing LAB as L. brevis strains, and designated them as L. brevis 119-2 and L. brevis 119-6, respectively. L. brevis is a plant-associated LAB reported to exhibit probiotic functions, for example, GABA production (Yokoyama et al, 2002), hepatic disease prevention (Segawa et al, 2008b), and immune activity (Segawa et al, 2008a). In this context, L. brevis is an important species for the functional food industry.…”

Section: Introductionmentioning

confidence: 99%

Cholesterol-lowering Effects of Lactobacillus brevis Isolated from Turnip “Tsuda Kabu”

Watanabe

Katšube

Sonomoto

2012

FSTR

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To develop new functional foods for the prevention of atherosclerosis, we evaluated the cholesterollowering effects of several strains of Lactobacillus (L.) brevis. These strains included the γ-amino butyric acid-producing strains L. brevis 119-2 and L. brevis 119-6, isolated from turnip "tsuda kabu" and pickled turnip "tsuda kabu zuke", respectively. To evaluate the cholesterol-lowering effects of L. brevis in vitro and to examine potential mechanisms of this property, we evaluated changes in levels of cholesterol, sodium taurocholate, and cholic acid in growth medium containing cholesterol and sodium taurocholate. Moreover, to assess the potential of L. brevis 119-2 and L. brevis 119-6 for probiotic use, we examined the tolerance of L. brevis to artificial digestive fluid and its adherence to epithelial cells. Our results indicate that L. brevis 119-2 incorporates cholesterol from the medium into the cell, and that L. brevis 119-2 and L. brevis 119-6 are probiotic bacteria. Therefore, we propose that viable cells of L. brevis 119-2 can reach the small intestine, where they can inhibit intestinal absorption of cholesterol in vivo by incorporation of cholesterol into the cell.

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Oral administration of heat-killed Lactobacillus brevis SBC8803 ameliorates alcoholic liver disease in ethanol-containing diet-fed C57BL/6N mice

Cited by 102 publications

References 35 publications

CD36-deficient mice are resistant to alcohol- and high-carbohydrate-induced hepatic steatosis

CD36-deficient mice are resistant to alcohol- and high-carbohydrate-induced hepatic steatosis

Effects of probiotics on methionine cholinedeficient diet-induced steatohepatitis in rats

Cholesterol-lowering Effects of Lactobacillus brevis Isolated from Turnip “Tsuda Kabu”

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