Preventive or Curative Administration of Taurine Regulates Lipid Metabolism in the Liver of Rats with Alcoholic Liver Disease

Tang, Riyi; Yang, Qihui; Lin, Shumei; Feng, Ying; Yang, Jiancheng; Lv, Qiufeng; Wu, Guanghui; Hu, Jianmin

doi:10.1007/978-981-13-8023-5_11

Cited by 14 publications

(11 citation statements)

References 43 publications

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“…FAS is a multienzyme protein catalysing fatty acid synthesis. 38 Our results demonstrated that SREBP-1C , HMGCR and FAS , which promote lipid synthesis, were markedly elevated by the HFD; however, aged LPT suppressed these changes. The HFD increased the SREBP-1C , HMGCR and FAS mRNA levels in the liver, identical to the results of previous studies.…”

Section: Discussionmentioning

confidence: 47%

“…36,37 HMGR is the ratecontrolling enzyme in the mevalonate pathway, catalysing the conversion of HMG-CoA to mevalonic acid, which is a necessary step in the production of cholesterol. 38 The increased level of HMGR in the HFD mouse liver corresponds to increased cholesterogenesis, as indicated by the higher contents of total cholesterol (TC) and LDL cholesterol (LDL-C) in the plasma. 39 FAS is a multienzyme protein catalysing fatty acid synthesis.…”

Section: Discussionmentioning

confidence: 99%

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Untargeted metabolomic and lipid metabolism-related gene expression analyses of the effects and mechanism of aged Liupao tea treatment in HFD-induced obese mice

Zhang

et al. 2021

RSC Adv.

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Section: Discussionmentioning

confidence: 47%

Section: Discussionmentioning

confidence: 99%

Untargeted metabolomic and lipid metabolism-related gene expression analyses of the effects and mechanism of aged Liupao tea treatment in HFD-induced obese mice

Zhang

et al. 2021

RSC Adv.

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“…Mechanistically, taurine inhibits cholesterol synthesis by AMPK-SREBP2-3-hydroxyl-3-methylglutaryl-CoA reductase (HMGCR). It also serves as a direct ligand of liver X receptor α (LXRα) and elevates the hepatic low-density lipoprotein (LDL) receptor [ 76 , 103 , 105 ], regulating the reverse cholesterol transport [ 106 ]. Upon accumulation in the liver, taurine supports the conversion of cholesterol into BAs via enhancement of the cholesterol 7α-hydroxylase (CYP7A1) enzyme [ 94 , 103 , 105 , 107 , 108 , 109 ].…”

Section: Taurinementioning

confidence: 99%

“…It also serves as a direct ligand of liver X receptor α (LXRα) and elevates the hepatic low-density lipoprotein (LDL) receptor [ 76 , 103 , 105 ], regulating the reverse cholesterol transport [ 106 ]. Upon accumulation in the liver, taurine supports the conversion of cholesterol into BAs via enhancement of the cholesterol 7α-hydroxylase (CYP7A1) enzyme [ 94 , 103 , 105 , 107 , 108 , 109 ]. In addition to regulating BAs synthesis, taurine also serves as a conjugation substrate for BAs, substantially changing their properties [ 110 ].…”

Section: Taurinementioning

confidence: 99%

Versatile Triad Alliance: Bile Acid, Taurine and Microbiota

Duszka

2022

Cells

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Taurine is the most abundant free amino acid in the body, and is mainly derived from the diet, but can also be produced endogenously from cysteine. It plays multiple essential roles in the body, including development, energy production, osmoregulation, prevention of oxidative stress, and inflammation. Taurine is also crucial as a molecule used to conjugate bile acids (BAs). In the gastrointestinal tract, BAs deconjugation by enteric bacteria results in high levels of unconjugated BAs and free taurine. Depending on conjugation status and other bacterial modifications, BAs constitute a pool of related but highly diverse molecules, each with different properties concerning solubility and toxicity, capacity to activate or inhibit receptors of BAs, and direct and indirect impact on microbiota and the host, whereas free taurine has a largely protective impact on the host, serves as a source of energy for microbiota, regulates bacterial colonization and defends from pathogens. Several remarkable examples of the interaction between taurine and gut microbiota have recently been described. This review will introduce the necessary background information and lay out the latest discoveries in the interaction of the co-reliant triad of BAs, taurine, and microbiota.

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“…Increasing evidence indicates that proinflammatory cytokines, such as TNF-α, IL-1β and IL-6, can induce inflammatory responses and aggravate inflammatory development in ALD [26]. It has been reported that SREBP-1c is elevated in ALD and PPAR-α is decreased in ALD, but both are associated with liver damage [27]. It is…”

Section: Discussionmentioning

confidence: 99%

Honokiol Inhibits the Inflammatory Response and Lipid Metabolism Disorder by Inhibiting p38α in Alcoholic Liver Disease

et al. 2022

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Alcoholic liver disease (ALD) is one of the leading causes of liver-related morbidity and mortality worldwide, but effective treatments are still lacking. Honokiol, a lignin-type natural compound isolated from the leaves and bark of Magnolia plants, has been widely studied for its beneficial effects on several chronic diseases. Accumulating studies have revealed that honokiol displays a potential therapeutic effect on ALD. In this study, the protective activity of honokiol on ALD was confirmed due to its significant inhibitory activity on the expression level of inflammatory cytokines (such as TNF-α, IL-6 and IL-1β) in EtOH-fed mice and in EtOH-induced AML-12 cells. Meanwhile, the expression of the lipid metabolic parameter SREBP-1c was also reduced. However, PPAR-α was increased in animal and cell experiments, which indicated that the activity of honokiol was related to its regulated activity on lipid metabolism. The findings also showed that honokiol significantly inhibited the expression level of p38α in vivo and in vitro. Blocking p38α inhibited the expression levels of TNF-α, IL-6, IL-1β and SREBP-1c but promoted the expression of PPAR-α compared with the honokiol-treated group. Moreover, forced expression of p38α further produced the opposite effect on inflammatory cytokines and lipid metabolism indicators. p38α has been related to the activation of NF-κB. In our study, honokiol significantly inhibited the phosphorylation and activation of NF-κB-pIKKα mediated by p38α. In conclusion, the results suggest that honokiol may be an effective regulator of p38α by downregulating the NF-κB pathway, thereby reducing the inflammatory response and lipid metabolism disorder in ALD.

show abstract

Preventive or Curative Administration of Taurine Regulates Lipid Metabolism in the Liver of Rats with Alcoholic Liver Disease

Cited by 14 publications

References 43 publications

Untargeted metabolomic and lipid metabolism-related gene expression analyses of the effects and mechanism of aged Liupao tea treatment in HFD-induced obese mice

Untargeted metabolomic and lipid metabolism-related gene expression analyses of the effects and mechanism of aged Liupao tea treatment in HFD-induced obese mice

Versatile Triad Alliance: Bile Acid, Taurine and Microbiota

Honokiol Inhibits the Inflammatory Response and Lipid Metabolism Disorder by Inhibiting p38α in Alcoholic Liver Disease

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