Preventing non-alcoholic fatty liver disease through Lactobacillus johnsonii BS15 by attenuating inflammation and mitochondrial injury and improving gut environment in obese mice
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- 英文论文题名：Preventing non-alcoholic fatty liver disease through Lactobacillus johnsonii BS15 by attenuating inflammation and mitochondrial injury and improving gut environment in obese mice
- 论文作者：Jinge Xin ; Dong Zeng ; Hesong Wang ; Xueqin Ni ; Dan Yi ; Kangcheng Pan ; Bo Jing
- 英文论文作者：Jinge Xin ; Dong Zeng ; Hesong Wang ; Xueqin Ni ; Dan Yi ; Kangcheng Pan ; Bo Jing ; Animal Microecology Institute ; College of Veterinary Medicine ; Sichuan Agricultural University ; Key Laboratory of Animal Disease and Human Health of Sichuan Province
- 年：2016
- 作者机构：Animal Microecology Institute,College of Veterinary Medicine,Sichuan Agricultural University;Key Laboratory of Animal Disease and Human Health of Sichuan Province;
- 英文论文关键词：Lactobacillus johnsonii ; non-alcoholic fatty liver disease ; intestinal permeability ; hepatocyte apoptosis ; hepatic inflammation ; oxidative stress
- 会议召开时间：2016-11-04
- 会议录名称：中国畜牧兽医学会动物微生态学分会第五届第十二次全国学术研讨会论文集
- 语种：英文
- 分类号：R589.2;R575.5
- 学会代码：ZGXJ
- 会议名称：中国畜牧兽医学会动物微生态学分会第五届第十二次全国学术研讨会
- 会议地点：中国山东青岛
- 主办单位：中国畜牧兽医学会动物微生态学分会
- 学会名称：中国畜牧兽医学会
- 页数：1
- 文件大小：69k
- 原文格式：O
- 会议级别：全国
摘要
The increasing prevalence of obesity worldwide is associated with a parallel increase in non-alcoholic fatty liver disease(NAFLD).To investigate the effect of Lactobacillus johnsonii BS 15 on NAFLD,120 male ICR mice were randomly divided into four groups and administrated with BS 15(2×10~7 cfu/0.2 mL or 2×10~8 cfu/0.2 mL)or phosphate buffered saline(PBS) throughout a 17-week experimental period.The mice were fed with normal chow diet(NCD) five weeks before the experimental period.Afterward,with the exception of the PBS group,NCD was changed into high-fat diet(HFD) for the remaining experimental period.Results showed that BS15-treated HFD mice were protected from hepatic steatosis and hepatocyte apoptosis.BS15 exhibited a positive effect on liver lipid peroxidation through an anti-oxidative stress activity by enhancing the liver antioxidant defense system.In addition,BS15 inhibited the insulin resistance;decreased the mRNA levels of acetyl-CoA carboxylase 1,fatty acid synthase,and peroxisome proliferator-activated receptor y;and increased the expression of the fasting-induced adipose factor in livers.Meanwhile,BS 15 attenuated mitochondria abnormalities when the content of uncoupling protein-2 decreased and cytochrome c increased in NAFLD mice.BS 15 also reduced the level of serum lipopolysaccharide in NAFLD mice by lowering the intestinal permeability and adjusting gut flora,followed by the downregulation of the TNFα mRNA level in liver and the serum level of C-reactive protein.These findings suggest that BS15 may be effective in preventing NAFLD induced by HFD.
The increasing prevalence of obesity worldwide is associated with a parallel increase in non-alcoholic fatty liver disease(NAFLD).To investigate the effect of Lactobacillus johnsonii BS 15 on NAFLD,120 male ICR mice were randomly divided into four groups and administrated with BS 15(2×10~7 cfu/0.2 mL or 2×10~8 cfu/0.2 mL)or phosphate buffered saline(PBS) throughout a 17-week experimental period.The mice were fed with normal chow diet(NCD) five weeks before the experimental period.Afterward,with the exception of the PBS group,NCD was changed into high-fat diet(HFD) for the remaining experimental period.Results showed that BS15-treated HFD mice were protected from hepatic steatosis and hepatocyte apoptosis.BS15 exhibited a positive effect on liver lipid peroxidation through an anti-oxidative stress activity by enhancing the liver antioxidant defense system.In addition,BS15 inhibited the insulin resistance;decreased the mRNA levels of acetyl-CoA carboxylase 1,fatty acid synthase,and peroxisome proliferator-activated receptor y;and increased the expression of the fasting-induced adipose factor in livers.Meanwhile,BS 15 attenuated mitochondria abnormalities when the content of uncoupling protein-2 decreased and cytochrome c increased in NAFLD mice.BS 15 also reduced the level of serum lipopolysaccharide in NAFLD mice by lowering the intestinal permeability and adjusting gut flora,followed by the downregulation of the TNFα mRNA level in liver and the serum level of C-reactive protein.These findings suggest that BS15 may be effective in preventing NAFLD induced by HFD.
The increasing prevalence of obesity worldwide is associated with a parallel increase in non-alcoholic fatty liver disease(NAFLD).To investigate the effect of Lactobacillus johnsonii BS 15 on NAFLD,120 male ICR mice were randomly divided into four groups and administrated with BS 15(2×10~7 cfu/0.2 mL or 2×10~8 cfu/0.2 mL)or phosphate buffered saline(PBS) throughout a 17-week experimental period.The mice were fed with normal chow diet(NCD) five weeks before the experimental period.Afterward,with the exception of the PBS group,NCD was changed into high-fat diet(HFD) for the remaining experimental period.Results showed that BS15-treated HFD mice were protected from hepatic steatosis and hepatocyte apoptosis.BS15 exhibited a positive effect on liver lipid peroxidation through an anti-oxidative stress activity by enhancing the liver antioxidant defense system.In addition,BS15 inhibited the insulin resistance;decreased the mRNA levels of acetyl-CoA carboxylase 1,fatty acid synthase,and peroxisome proliferator-activated receptor y;and increased the expression of the fasting-induced adipose factor in livers.Meanwhile,BS 15 attenuated mitochondria abnormalities when the content of uncoupling protein-2 decreased and cytochrome c increased in NAFLD mice.BS 15 also reduced the level of serum lipopolysaccharide in NAFLD mice by lowering the intestinal permeability and adjusting gut flora,followed by the downregulation of the TNFα mRNA level in liver and the serum level of C-reactive protein.These findings suggest that BS15 may be effective in preventing NAFLD induced by HFD.
引文
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Almanza-Perez J,Alarcon-Aguilar F,Blancas-Flores G,Campos-Sepulveda A,Roman-Ramos R,Garcia-Macedo R,Cruz M(2010)Glycine regulates inflammatory markers modifying the energetic balance through PPAR and UCP-2.Biomed Pharmacother 64:534-540.
Assimakopoulos SF(2013)On the role of intestinal hyperpermeability in complications of cirrhosis.Liver Int 33:495.doi:10.1111/liv.l2094
Almanza-Perez J,Alarcon-Aguilar F,Blancas-Flores G,Campos-Sepulveda A,Roman-Ramos R,Garcia-Macedo R,Cruz M(2010)Glycine regulates inflammatory markers modifying the energetic balance through PPAR and UCP-2.Biomed Pharmacother 64:534-540.
Assimakopoulos SF(2013)On the role of intestinal hyperpermeability in complications of cirrhosis.Liver Int 33:495.doi:10.1111/liv.l2094