The Experts below are selected from a list of 15 Experts worldwide ranked by ideXlab platform
Lin Shimei - One of the best experts on this subject based on the ideXlab platform.
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Effects of Dietary Lipid Level and Compound Lipotropic Agent on Growth Performance and Metabolic and Antioxidant Indices in Hepatopancreas of Tilapia
Chinese Journal of Animal Nutrition, 2010Co-Authors: Lin ShimeiAbstract:A feeding experiment was conducted to investigate the effects of dietary lipid level and compound Lipotropic Agent on growth performance,body composition and activities of metabolism related enzymes and antioxidant enzymes in hepatopancreas of tilapia.Four practical diets were formulated to contain 3 levels of lipid(4.5%,6.5% and 8.5%) and a level of compound Lipotropic Agent(0.1% compound Lipotropic Agent and 8.5% lipid) on an equal nitrogen basis(CP=30%).Three hundred and sixty hybrid tilapia(Oreochromis niloticus×O.aureus) with an initial body weight of(4.21±0.09) g were randomly divided into 4 groups(with 3 replicates of 20 fish) and each group were fed 1 experimental diet.The experiment lasted for 8 weeks.The results showed as follows: with the dietary lipid level increasing,the specific growth rate(SGR) and protein efficiency ratio(PER) were significantly increased(P0.05),and the feed conversion ratio(FCR) was significantly decreased(P0.05);supplemented with 1% compound Lipotropic Agent in 8.5% lipid diet could significantly increase PER(P0.05),and significantly decrease the FCR(P0.05).Fish fed the diet containing 8.5% lipid could significantly increase the hepatopancreas lipid and body lipid contents(P0.05),but the diet supplemented with 0.1% compound Lipotropic Agent could significantly decreased the hepatopancreas lipid and body lipid contents(P0.05).With the dietary lipid level increasing,the activities of glutamyl oxaloacetic transaminase(GOT) and glutamyl pyruvic transaminase(GPT) in hepatopancreas were significantly decreased(P0.05),and the catalyse(CAT) activity and MDA content were significantly increased(P0.05);supplemented with compound Lipotropic Agent in 8.5% lipid diet could significantly increase the activities of GOT and GPT(P0.05),and significantly decrease the catalyse(CAT) activity and MDA content(P0.05).The results suggest that increasing dietary lipid level can significantly improve the growth performance of tilapia,but the higher lipid levels can damage the physiological function of liver.The results also suggest that 0.1% compound Lipotropic Agent supplementation in diet can improve the physiological function of liver and growth of tilapia.Therefore,compound Lipotropic Agent can be added into the diet of tilapia as a safe and efficacious liver protecting additive.
Zhu Hui-lian - One of the best experts on this subject based on the ideXlab platform.
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Betaine attenuates hepatic steatosis by reducing methylation of the MTTP promoter and elevating genomic methylation in mice fed a high-fat diet
ELSEVIER SCIENCE INC, 2014Co-Authors: Wang Li-jun, Zhang Hong-wei, Zhou Jing-ya, Liu Yan, Yang Yang, Chen Xiao-ling, Zhu Cui-hong, Zheng Rui-dan, Ling Wen-hua, Zhu Hui-lianAbstract:National Natural Science Foundation of China [81072302, 81273050]; Science and Technology Project of Guangzhou, China [201300000148]; Danone Institute China Diet and Nutrition Research and CommunicationAberrant DNA methylation contributes to the abnormality of hepatic gene expression, one of the main factors in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Betaine is a methyl donor and has been considered to be a Lipotropic Agent. However, whether betaine supplementation improves NAFLD via its effect on the DNA methylation of specific genes and the genome has not been explored. Male C57BL/6 mice were fed either a control diet or high-fat diet (HFD) supplemented with 0%, 1% and 2% betaine in water (wt/vol) for 12 weeks. Betaine supplementation ameliorated HFD-induced hepatic steatosis in a dose-dependent manner. HFD up-regulated FAS and ACOX messenger RNA (mRNA) expression and down-regulated PPAR alpha, ApoB and MTTP mRNA expression; however, these alterations were reversed by betaine supplementation, except ApoB. MTTP mRNA expression was negatively correlated with the DNA methylation of its CpG sites at -184, -156, -63 and -60. Methylation of these CpG sites was lower in both the 1% and 2% betaine-supplemented groups than in the HFD group (averages; 25.55% and 14.33% vs. 30.13%). In addition, both 1% and 2% betaine supplementation significantly restored the methylation capacity [S-adenosylmethionine (SAM) concentration and SAM/S-adenosylhomocysteine ratios] and genomic methylation level, which had been decreased by HFD (0.37% and 0.47% vs. 0.25%). These results suggest that the regulation of aberrant DNA methylation by betaine might be a possible mechanism of the improvements in NAFLD upon betaine supplementation. (C) 2014 Elsevier Inc. All rights reserved
Wang Li-jun - One of the best experts on this subject based on the ideXlab platform.
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Betaine attenuates hepatic steatosis by reducing methylation of the MTTP promoter and elevating genomic methylation in mice fed a high-fat diet
ELSEVIER SCIENCE INC, 2014Co-Authors: Wang Li-jun, Zhang Hong-wei, Zhou Jing-ya, Liu Yan, Yang Yang, Chen Xiao-ling, Zhu Cui-hong, Zheng Rui-dan, Ling Wen-hua, Zhu Hui-lianAbstract:National Natural Science Foundation of China [81072302, 81273050]; Science and Technology Project of Guangzhou, China [201300000148]; Danone Institute China Diet and Nutrition Research and CommunicationAberrant DNA methylation contributes to the abnormality of hepatic gene expression, one of the main factors in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Betaine is a methyl donor and has been considered to be a Lipotropic Agent. However, whether betaine supplementation improves NAFLD via its effect on the DNA methylation of specific genes and the genome has not been explored. Male C57BL/6 mice were fed either a control diet or high-fat diet (HFD) supplemented with 0%, 1% and 2% betaine in water (wt/vol) for 12 weeks. Betaine supplementation ameliorated HFD-induced hepatic steatosis in a dose-dependent manner. HFD up-regulated FAS and ACOX messenger RNA (mRNA) expression and down-regulated PPAR alpha, ApoB and MTTP mRNA expression; however, these alterations were reversed by betaine supplementation, except ApoB. MTTP mRNA expression was negatively correlated with the DNA methylation of its CpG sites at -184, -156, -63 and -60. Methylation of these CpG sites was lower in both the 1% and 2% betaine-supplemented groups than in the HFD group (averages; 25.55% and 14.33% vs. 30.13%). In addition, both 1% and 2% betaine supplementation significantly restored the methylation capacity [S-adenosylmethionine (SAM) concentration and SAM/S-adenosylhomocysteine ratios] and genomic methylation level, which had been decreased by HFD (0.37% and 0.47% vs. 0.25%). These results suggest that the regulation of aberrant DNA methylation by betaine might be a possible mechanism of the improvements in NAFLD upon betaine supplementation. (C) 2014 Elsevier Inc. All rights reserved
Zhang Hong-wei - One of the best experts on this subject based on the ideXlab platform.
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Betaine attenuates hepatic steatosis by reducing methylation of the MTTP promoter and elevating genomic methylation in mice fed a high-fat diet
ELSEVIER SCIENCE INC, 2014Co-Authors: Wang Li-jun, Zhang Hong-wei, Zhou Jing-ya, Liu Yan, Yang Yang, Chen Xiao-ling, Zhu Cui-hong, Zheng Rui-dan, Ling Wen-hua, Zhu Hui-lianAbstract:National Natural Science Foundation of China [81072302, 81273050]; Science and Technology Project of Guangzhou, China [201300000148]; Danone Institute China Diet and Nutrition Research and CommunicationAberrant DNA methylation contributes to the abnormality of hepatic gene expression, one of the main factors in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Betaine is a methyl donor and has been considered to be a Lipotropic Agent. However, whether betaine supplementation improves NAFLD via its effect on the DNA methylation of specific genes and the genome has not been explored. Male C57BL/6 mice were fed either a control diet or high-fat diet (HFD) supplemented with 0%, 1% and 2% betaine in water (wt/vol) for 12 weeks. Betaine supplementation ameliorated HFD-induced hepatic steatosis in a dose-dependent manner. HFD up-regulated FAS and ACOX messenger RNA (mRNA) expression and down-regulated PPAR alpha, ApoB and MTTP mRNA expression; however, these alterations were reversed by betaine supplementation, except ApoB. MTTP mRNA expression was negatively correlated with the DNA methylation of its CpG sites at -184, -156, -63 and -60. Methylation of these CpG sites was lower in both the 1% and 2% betaine-supplemented groups than in the HFD group (averages; 25.55% and 14.33% vs. 30.13%). In addition, both 1% and 2% betaine supplementation significantly restored the methylation capacity [S-adenosylmethionine (SAM) concentration and SAM/S-adenosylhomocysteine ratios] and genomic methylation level, which had been decreased by HFD (0.37% and 0.47% vs. 0.25%). These results suggest that the regulation of aberrant DNA methylation by betaine might be a possible mechanism of the improvements in NAFLD upon betaine supplementation. (C) 2014 Elsevier Inc. All rights reserved
Ling Wen-hua - One of the best experts on this subject based on the ideXlab platform.
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Betaine attenuates hepatic steatosis by reducing methylation of the MTTP promoter and elevating genomic methylation in mice fed a high-fat diet
ELSEVIER SCIENCE INC, 2014Co-Authors: Wang Li-jun, Zhang Hong-wei, Zhou Jing-ya, Liu Yan, Yang Yang, Chen Xiao-ling, Zhu Cui-hong, Zheng Rui-dan, Ling Wen-hua, Zhu Hui-lianAbstract:National Natural Science Foundation of China [81072302, 81273050]; Science and Technology Project of Guangzhou, China [201300000148]; Danone Institute China Diet and Nutrition Research and CommunicationAberrant DNA methylation contributes to the abnormality of hepatic gene expression, one of the main factors in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Betaine is a methyl donor and has been considered to be a Lipotropic Agent. However, whether betaine supplementation improves NAFLD via its effect on the DNA methylation of specific genes and the genome has not been explored. Male C57BL/6 mice were fed either a control diet or high-fat diet (HFD) supplemented with 0%, 1% and 2% betaine in water (wt/vol) for 12 weeks. Betaine supplementation ameliorated HFD-induced hepatic steatosis in a dose-dependent manner. HFD up-regulated FAS and ACOX messenger RNA (mRNA) expression and down-regulated PPAR alpha, ApoB and MTTP mRNA expression; however, these alterations were reversed by betaine supplementation, except ApoB. MTTP mRNA expression was negatively correlated with the DNA methylation of its CpG sites at -184, -156, -63 and -60. Methylation of these CpG sites was lower in both the 1% and 2% betaine-supplemented groups than in the HFD group (averages; 25.55% and 14.33% vs. 30.13%). In addition, both 1% and 2% betaine supplementation significantly restored the methylation capacity [S-adenosylmethionine (SAM) concentration and SAM/S-adenosylhomocysteine ratios] and genomic methylation level, which had been decreased by HFD (0.37% and 0.47% vs. 0.25%). These results suggest that the regulation of aberrant DNA methylation by betaine might be a possible mechanism of the improvements in NAFLD upon betaine supplementation. (C) 2014 Elsevier Inc. All rights reserved