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Jiyoung Lee - One of the best experts on this subject based on the ideXlab platform.
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nicotinamide riboside an nad precursor attenuates the development of Liver Fibrosis in a diet induced mouse model of Liver Fibrosis
Biochimica et Biophysica Acta, 2019Co-Authors: Tho X Pham, Minkyung Bae, Mibo Kim, Yoojin Lee, Hyunju Kang, Youngki Park, Jiyoung LeeAbstract:Abstract Objective Liver Fibrosis is part of the non-alcoholic fatty Liver disease (NAFLD) spectrum, which currently has no approved pharmacological treatment. In this study, we investigated whether supplementation of nicotinamide riboside (NR), a nicotinamide adenine dinucleotide (NAD+) precursor, can reduce the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. Methods Male C57BL/6 J mice were fed a low-fat control (LF), a high-fat/high-sucrose/high-cholesterol control (HF) or a HF diet supplemented with NR at 400 mg/kg/day (HF-NR) for 20 weeks. Features of Liver Fibrosis were assessed by histological and biochemical analyses. Whole-body energy metabolism was also assessed using indirect calorimetry. Primary mouse and human hepatic stellate cells were used to determine the anti-fibrogenic effects of NR in vitro. Results NR supplementation significantly reduced body weight of mice only 7 weeks after mice were on the supplementation, but did not attenuate serum alanine aminotransferase levels, Liver steatosis, or Liver inflammation. However, NR markedly reduced collagen accumulation in the Liver. RNA-Seq analysis suggested that the expression of genes involved in NAD+ metabolism is altered in activated hepatic stellate cells (HSCs) compared to quiescent HSCs. NR inhibited the activation of HSCs in primary mouse and human HSCs. Indirect calorimetry showed that NR increased energy expenditure, likely by upregulation of β-oxidation in skeletal muscle and brown adipose tissue. Conclusion NR attenuated HSC activation, leading to reduced Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. The data suggest that NR may be developed as a potential preventative for human Liver Fibrosis.
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Nicotinamide riboside, an NAD+ precursor, attenuates the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis.
Biochimica et biophysica acta. Molecular basis of disease, 2019Co-Authors: Tho X Pham, Minkyung Bae, Mibo Kim, Yoojin Lee, Hyunju Kang, Youngki Park, Jiyoung LeeAbstract:Liver Fibrosis is part of the non-alcoholic fatty Liver disease (NAFLD) spectrum, which currently has no approved pharmacological treatment. In this study, we investigated whether supplementation of nicotinamide riboside (NR), a nicotinamide adenine dinucleotide (NAD+) precursor, can reduce the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. Male C57BL/6 J mice were fed a low-fat control (LF), a high-fat/high-sucrose/high-cholesterol control (HF) or a HF diet supplemented with NR at 400 mg/kg/day (HF-NR) for 20 weeks. Features of Liver Fibrosis were assessed by histological and biochemical analyses. Whole-body energy metabolism was also assessed using indirect calorimetry. Primary mouse and human hepatic stellate cells were used to determine the anti-fibrogenic effects of NR in vitro. NR supplementation significantly reduced body weight of mice only 7 weeks after mice were on the supplementation, but did not attenuate serum alanine aminotransferase levels, Liver steatosis, or Liver inflammation. However, NR markedly reduced collagen accumulation in the Liver. RNA-Seq analysis suggested that the expression of genes involved in NAD+ metabolism is altered in activated hepatic stellate cells (HSCs) compared to quiescent HSCs. NR inhibited the activation of HSCs in primary mouse and human HSCs. Indirect calorimetry showed that NR increased energy expenditure, likely by upregulation of β-oxidation in skeletal muscle and brown adipose tissue. NR attenuated HSC activation, leading to reduced Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. The data suggest that NR may be developed as a potential preventative for human Liver Fibrosis. Copyright © 2019 Elsevier B.V. All rights reserved.
Tho X Pham - One of the best experts on this subject based on the ideXlab platform.
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nicotinamide riboside an nad precursor attenuates the development of Liver Fibrosis in a diet induced mouse model of Liver Fibrosis
Biochimica et Biophysica Acta, 2019Co-Authors: Tho X Pham, Minkyung Bae, Mibo Kim, Yoojin Lee, Hyunju Kang, Youngki Park, Jiyoung LeeAbstract:Abstract Objective Liver Fibrosis is part of the non-alcoholic fatty Liver disease (NAFLD) spectrum, which currently has no approved pharmacological treatment. In this study, we investigated whether supplementation of nicotinamide riboside (NR), a nicotinamide adenine dinucleotide (NAD+) precursor, can reduce the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. Methods Male C57BL/6 J mice were fed a low-fat control (LF), a high-fat/high-sucrose/high-cholesterol control (HF) or a HF diet supplemented with NR at 400 mg/kg/day (HF-NR) for 20 weeks. Features of Liver Fibrosis were assessed by histological and biochemical analyses. Whole-body energy metabolism was also assessed using indirect calorimetry. Primary mouse and human hepatic stellate cells were used to determine the anti-fibrogenic effects of NR in vitro. Results NR supplementation significantly reduced body weight of mice only 7 weeks after mice were on the supplementation, but did not attenuate serum alanine aminotransferase levels, Liver steatosis, or Liver inflammation. However, NR markedly reduced collagen accumulation in the Liver. RNA-Seq analysis suggested that the expression of genes involved in NAD+ metabolism is altered in activated hepatic stellate cells (HSCs) compared to quiescent HSCs. NR inhibited the activation of HSCs in primary mouse and human HSCs. Indirect calorimetry showed that NR increased energy expenditure, likely by upregulation of β-oxidation in skeletal muscle and brown adipose tissue. Conclusion NR attenuated HSC activation, leading to reduced Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. The data suggest that NR may be developed as a potential preventative for human Liver Fibrosis.
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Nicotinamide riboside, an NAD+ precursor, attenuates the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis.
Biochimica et biophysica acta. Molecular basis of disease, 2019Co-Authors: Tho X Pham, Minkyung Bae, Mibo Kim, Yoojin Lee, Hyunju Kang, Youngki Park, Jiyoung LeeAbstract:Liver Fibrosis is part of the non-alcoholic fatty Liver disease (NAFLD) spectrum, which currently has no approved pharmacological treatment. In this study, we investigated whether supplementation of nicotinamide riboside (NR), a nicotinamide adenine dinucleotide (NAD+) precursor, can reduce the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. Male C57BL/6 J mice were fed a low-fat control (LF), a high-fat/high-sucrose/high-cholesterol control (HF) or a HF diet supplemented with NR at 400 mg/kg/day (HF-NR) for 20 weeks. Features of Liver Fibrosis were assessed by histological and biochemical analyses. Whole-body energy metabolism was also assessed using indirect calorimetry. Primary mouse and human hepatic stellate cells were used to determine the anti-fibrogenic effects of NR in vitro. NR supplementation significantly reduced body weight of mice only 7 weeks after mice were on the supplementation, but did not attenuate serum alanine aminotransferase levels, Liver steatosis, or Liver inflammation. However, NR markedly reduced collagen accumulation in the Liver. RNA-Seq analysis suggested that the expression of genes involved in NAD+ metabolism is altered in activated hepatic stellate cells (HSCs) compared to quiescent HSCs. NR inhibited the activation of HSCs in primary mouse and human HSCs. Indirect calorimetry showed that NR increased energy expenditure, likely by upregulation of β-oxidation in skeletal muscle and brown adipose tissue. NR attenuated HSC activation, leading to reduced Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. The data suggest that NR may be developed as a potential preventative for human Liver Fibrosis. Copyright © 2019 Elsevier B.V. All rights reserved.
Minkyung Bae - One of the best experts on this subject based on the ideXlab platform.
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nicotinamide riboside an nad precursor attenuates the development of Liver Fibrosis in a diet induced mouse model of Liver Fibrosis
Biochimica et Biophysica Acta, 2019Co-Authors: Tho X Pham, Minkyung Bae, Mibo Kim, Yoojin Lee, Hyunju Kang, Youngki Park, Jiyoung LeeAbstract:Abstract Objective Liver Fibrosis is part of the non-alcoholic fatty Liver disease (NAFLD) spectrum, which currently has no approved pharmacological treatment. In this study, we investigated whether supplementation of nicotinamide riboside (NR), a nicotinamide adenine dinucleotide (NAD+) precursor, can reduce the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. Methods Male C57BL/6 J mice were fed a low-fat control (LF), a high-fat/high-sucrose/high-cholesterol control (HF) or a HF diet supplemented with NR at 400 mg/kg/day (HF-NR) for 20 weeks. Features of Liver Fibrosis were assessed by histological and biochemical analyses. Whole-body energy metabolism was also assessed using indirect calorimetry. Primary mouse and human hepatic stellate cells were used to determine the anti-fibrogenic effects of NR in vitro. Results NR supplementation significantly reduced body weight of mice only 7 weeks after mice were on the supplementation, but did not attenuate serum alanine aminotransferase levels, Liver steatosis, or Liver inflammation. However, NR markedly reduced collagen accumulation in the Liver. RNA-Seq analysis suggested that the expression of genes involved in NAD+ metabolism is altered in activated hepatic stellate cells (HSCs) compared to quiescent HSCs. NR inhibited the activation of HSCs in primary mouse and human HSCs. Indirect calorimetry showed that NR increased energy expenditure, likely by upregulation of β-oxidation in skeletal muscle and brown adipose tissue. Conclusion NR attenuated HSC activation, leading to reduced Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. The data suggest that NR may be developed as a potential preventative for human Liver Fibrosis.
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Nicotinamide riboside, an NAD+ precursor, attenuates the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis.
Biochimica et biophysica acta. Molecular basis of disease, 2019Co-Authors: Tho X Pham, Minkyung Bae, Mibo Kim, Yoojin Lee, Hyunju Kang, Youngki Park, Jiyoung LeeAbstract:Liver Fibrosis is part of the non-alcoholic fatty Liver disease (NAFLD) spectrum, which currently has no approved pharmacological treatment. In this study, we investigated whether supplementation of nicotinamide riboside (NR), a nicotinamide adenine dinucleotide (NAD+) precursor, can reduce the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. Male C57BL/6 J mice were fed a low-fat control (LF), a high-fat/high-sucrose/high-cholesterol control (HF) or a HF diet supplemented with NR at 400 mg/kg/day (HF-NR) for 20 weeks. Features of Liver Fibrosis were assessed by histological and biochemical analyses. Whole-body energy metabolism was also assessed using indirect calorimetry. Primary mouse and human hepatic stellate cells were used to determine the anti-fibrogenic effects of NR in vitro. NR supplementation significantly reduced body weight of mice only 7 weeks after mice were on the supplementation, but did not attenuate serum alanine aminotransferase levels, Liver steatosis, or Liver inflammation. However, NR markedly reduced collagen accumulation in the Liver. RNA-Seq analysis suggested that the expression of genes involved in NAD+ metabolism is altered in activated hepatic stellate cells (HSCs) compared to quiescent HSCs. NR inhibited the activation of HSCs in primary mouse and human HSCs. Indirect calorimetry showed that NR increased energy expenditure, likely by upregulation of β-oxidation in skeletal muscle and brown adipose tissue. NR attenuated HSC activation, leading to reduced Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. The data suggest that NR may be developed as a potential preventative for human Liver Fibrosis. Copyright © 2019 Elsevier B.V. All rights reserved.
Mibo Kim - One of the best experts on this subject based on the ideXlab platform.
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nicotinamide riboside an nad precursor attenuates the development of Liver Fibrosis in a diet induced mouse model of Liver Fibrosis
Biochimica et Biophysica Acta, 2019Co-Authors: Tho X Pham, Minkyung Bae, Mibo Kim, Yoojin Lee, Hyunju Kang, Youngki Park, Jiyoung LeeAbstract:Abstract Objective Liver Fibrosis is part of the non-alcoholic fatty Liver disease (NAFLD) spectrum, which currently has no approved pharmacological treatment. In this study, we investigated whether supplementation of nicotinamide riboside (NR), a nicotinamide adenine dinucleotide (NAD+) precursor, can reduce the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. Methods Male C57BL/6 J mice were fed a low-fat control (LF), a high-fat/high-sucrose/high-cholesterol control (HF) or a HF diet supplemented with NR at 400 mg/kg/day (HF-NR) for 20 weeks. Features of Liver Fibrosis were assessed by histological and biochemical analyses. Whole-body energy metabolism was also assessed using indirect calorimetry. Primary mouse and human hepatic stellate cells were used to determine the anti-fibrogenic effects of NR in vitro. Results NR supplementation significantly reduced body weight of mice only 7 weeks after mice were on the supplementation, but did not attenuate serum alanine aminotransferase levels, Liver steatosis, or Liver inflammation. However, NR markedly reduced collagen accumulation in the Liver. RNA-Seq analysis suggested that the expression of genes involved in NAD+ metabolism is altered in activated hepatic stellate cells (HSCs) compared to quiescent HSCs. NR inhibited the activation of HSCs in primary mouse and human HSCs. Indirect calorimetry showed that NR increased energy expenditure, likely by upregulation of β-oxidation in skeletal muscle and brown adipose tissue. Conclusion NR attenuated HSC activation, leading to reduced Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. The data suggest that NR may be developed as a potential preventative for human Liver Fibrosis.
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Nicotinamide riboside, an NAD+ precursor, attenuates the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis.
Biochimica et biophysica acta. Molecular basis of disease, 2019Co-Authors: Tho X Pham, Minkyung Bae, Mibo Kim, Yoojin Lee, Hyunju Kang, Youngki Park, Jiyoung LeeAbstract:Liver Fibrosis is part of the non-alcoholic fatty Liver disease (NAFLD) spectrum, which currently has no approved pharmacological treatment. In this study, we investigated whether supplementation of nicotinamide riboside (NR), a nicotinamide adenine dinucleotide (NAD+) precursor, can reduce the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. Male C57BL/6 J mice were fed a low-fat control (LF), a high-fat/high-sucrose/high-cholesterol control (HF) or a HF diet supplemented with NR at 400 mg/kg/day (HF-NR) for 20 weeks. Features of Liver Fibrosis were assessed by histological and biochemical analyses. Whole-body energy metabolism was also assessed using indirect calorimetry. Primary mouse and human hepatic stellate cells were used to determine the anti-fibrogenic effects of NR in vitro. NR supplementation significantly reduced body weight of mice only 7 weeks after mice were on the supplementation, but did not attenuate serum alanine aminotransferase levels, Liver steatosis, or Liver inflammation. However, NR markedly reduced collagen accumulation in the Liver. RNA-Seq analysis suggested that the expression of genes involved in NAD+ metabolism is altered in activated hepatic stellate cells (HSCs) compared to quiescent HSCs. NR inhibited the activation of HSCs in primary mouse and human HSCs. Indirect calorimetry showed that NR increased energy expenditure, likely by upregulation of β-oxidation in skeletal muscle and brown adipose tissue. NR attenuated HSC activation, leading to reduced Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. The data suggest that NR may be developed as a potential preventative for human Liver Fibrosis. Copyright © 2019 Elsevier B.V. All rights reserved.
Yoojin Lee - One of the best experts on this subject based on the ideXlab platform.
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nicotinamide riboside an nad precursor attenuates the development of Liver Fibrosis in a diet induced mouse model of Liver Fibrosis
Biochimica et Biophysica Acta, 2019Co-Authors: Tho X Pham, Minkyung Bae, Mibo Kim, Yoojin Lee, Hyunju Kang, Youngki Park, Jiyoung LeeAbstract:Abstract Objective Liver Fibrosis is part of the non-alcoholic fatty Liver disease (NAFLD) spectrum, which currently has no approved pharmacological treatment. In this study, we investigated whether supplementation of nicotinamide riboside (NR), a nicotinamide adenine dinucleotide (NAD+) precursor, can reduce the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. Methods Male C57BL/6 J mice were fed a low-fat control (LF), a high-fat/high-sucrose/high-cholesterol control (HF) or a HF diet supplemented with NR at 400 mg/kg/day (HF-NR) for 20 weeks. Features of Liver Fibrosis were assessed by histological and biochemical analyses. Whole-body energy metabolism was also assessed using indirect calorimetry. Primary mouse and human hepatic stellate cells were used to determine the anti-fibrogenic effects of NR in vitro. Results NR supplementation significantly reduced body weight of mice only 7 weeks after mice were on the supplementation, but did not attenuate serum alanine aminotransferase levels, Liver steatosis, or Liver inflammation. However, NR markedly reduced collagen accumulation in the Liver. RNA-Seq analysis suggested that the expression of genes involved in NAD+ metabolism is altered in activated hepatic stellate cells (HSCs) compared to quiescent HSCs. NR inhibited the activation of HSCs in primary mouse and human HSCs. Indirect calorimetry showed that NR increased energy expenditure, likely by upregulation of β-oxidation in skeletal muscle and brown adipose tissue. Conclusion NR attenuated HSC activation, leading to reduced Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. The data suggest that NR may be developed as a potential preventative for human Liver Fibrosis.
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Nicotinamide riboside, an NAD+ precursor, attenuates the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis.
Biochimica et biophysica acta. Molecular basis of disease, 2019Co-Authors: Tho X Pham, Minkyung Bae, Mibo Kim, Yoojin Lee, Hyunju Kang, Youngki Park, Jiyoung LeeAbstract:Liver Fibrosis is part of the non-alcoholic fatty Liver disease (NAFLD) spectrum, which currently has no approved pharmacological treatment. In this study, we investigated whether supplementation of nicotinamide riboside (NR), a nicotinamide adenine dinucleotide (NAD+) precursor, can reduce the development of Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. Male C57BL/6 J mice were fed a low-fat control (LF), a high-fat/high-sucrose/high-cholesterol control (HF) or a HF diet supplemented with NR at 400 mg/kg/day (HF-NR) for 20 weeks. Features of Liver Fibrosis were assessed by histological and biochemical analyses. Whole-body energy metabolism was also assessed using indirect calorimetry. Primary mouse and human hepatic stellate cells were used to determine the anti-fibrogenic effects of NR in vitro. NR supplementation significantly reduced body weight of mice only 7 weeks after mice were on the supplementation, but did not attenuate serum alanine aminotransferase levels, Liver steatosis, or Liver inflammation. However, NR markedly reduced collagen accumulation in the Liver. RNA-Seq analysis suggested that the expression of genes involved in NAD+ metabolism is altered in activated hepatic stellate cells (HSCs) compared to quiescent HSCs. NR inhibited the activation of HSCs in primary mouse and human HSCs. Indirect calorimetry showed that NR increased energy expenditure, likely by upregulation of β-oxidation in skeletal muscle and brown adipose tissue. NR attenuated HSC activation, leading to reduced Liver Fibrosis in a diet-induced mouse model of Liver Fibrosis. The data suggest that NR may be developed as a potential preventative for human Liver Fibrosis. Copyright © 2019 Elsevier B.V. All rights reserved.
