Aurantio-Obtusin Attenuates Non-Alcoholic Fatty Liver Disease Through AMPK-Mediated Autophagy and Fatty Acid Oxidation Pathways

Zhou, Fei; Ding, Mingning; Gu, Yiqing; Fan, Guifang; Liu, Chuanyang; Li, Yijie; Sun, Rong; Wu, Jianzhi; Li, Jianchao; Xue, Xiaoyong; Li, Hongjuan; Li, Xiaojiaoyang

doi:10.3389/fphar.2021.826628

Cited by 22 publications

(15 citation statements)

References 47 publications

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“…Treatment with L. plantarum ZJUIDS14 induced a marked decrease in OGTT and ITT AUC values. Consistent with other studies (27)(28)(29), HFD significantly increased the levels of plasma TG, FFA, TC, and LDL-C. Moreover, the plasma levels of HDL-C were increased and TG, FFA, and LDL-C were distinctly reduced * P < 0.05, * * P < 0.01, * * * P < 0.001 vs NFD group; # P < 0.05, ## P < 0.01 vs HFD group.…”

Section: Discussionsupporting

confidence: 92%

Lactobacillus plantarum ZJUIDS14 alleviates non-alcoholic fatty liver disease in mice in association with modulation in the gut microbiota

Cao

Ding²,

Zhuge³

et al. 2023

Front. Nutr.

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This present study was designed to explore the protective role of Lactobacillus plantarum ZJUIDS14 against Non-alcoholic Fatty Liver Disease (NAFLD) in a high-fat-diet (HFD)-induced C57BL/6 mice model. The probiotic (109 CFU/every other day) was administered by oral gavage for 12 weeks. We found that L. plantarum ZJUIDS14 intervention significantly alleviated HFD related hepatic steatosis, liver damage, insulin resistance, and increased hepatic expression of peroxisome proliferator activated receptor α (PPAR-α) while stimulating the activation of AMP-activated protein kinase (AMPK). Furthermore, L. plantarum ZJUIDS14 improved mitochondrial function as reflected by an increase in dynamin related protein 1 (DRP1) and a decrease of proteins associated with oxidative phosphorylation (OXPHOS) after the treatment. Additionally, mice from the L. plantarum ZJUIDS14 group had a restored intestinal flora and homeostasis involving Coprostanoligenes group, Ruminococcaceae UCG-014, Allobaculum, Ruminiclostridium 1, and Roseburia. Meanwhile, these five genera exhibited a significant (negative or positive) association with ileum inflammation mRNA levels and SCFA contents, by Spearman’s correlation analysis. In general, our data demonstrated that L. plantarum ZJUIDS14 mitigates hepatic steatosis and liver damage induced by HFD. Specifically, they strengthened the integrity of the intestinal barrier, regulated gut microbiota, and improved mitochondrial function. Our data provide an experimental basis for L. plantarum ZJUIDS14 as a promising candidate to prevent NAFLD.

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Section: Discussionsupporting

confidence: 92%

Lactobacillus plantarum ZJUIDS14 alleviates non-alcoholic fatty liver disease in mice in association with modulation in the gut microbiota

Cao

Ding²,

Zhuge³

et al. 2023

Front. Nutr.

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“…New regulators involved in the regulation of peroxisomal β-oxidation have constantly been identified. AMPK, for example, promotes FAO by activating the expression of PPARα and ACOX1 [107,108], whereas mTOR promotes the accumulation of FAs by shutting down β-oxidation [109,110]. Hence, these are considered the AMPK-mTOR pathway for regulating β-oxidation [111].…”

Section: Othersmentioning

confidence: 99%

The Overlooked Transformation Mechanisms of VLCFAs: Peroxisomal β-Oxidation

Zong

Zhang

et al. 2022

Agriculture

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Beta-oxidation(β-oxidation) is an important metabolic process involving multiple steps by which fatty acid molecules are broken down to produce energy. The very long-chain fatty acids (VLCFAs), a type of fatty acid (FA), are usually highly toxic when free in vivo, and their oxidative metabolism depends on the peroxisomal β-oxidation. For a long time, although β-oxidation takes place in both mitochondria and peroxisomes, most studies have been keen to explore the mechanism of β-oxidation in mitochondria while ignoring the importance of peroxisomal β-oxidation. However, current studies indicate that it is hard to provide effective treatment for diseases caused by the disorder of peroxisomal β-oxidation, such as X-ALD, SCOX deficiency, and D-BP deficiency; thus, actions should be taken to solve this problem. Based on existing research results, this review will summarize the importance of peroxisomal β-oxidation and help further learning.

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“…The reduction of AMPK activity may further exacerbate the imbalance of lipid metabolism in the liver and the accumulation of hepatic lipids. On the one hand, reduced AMPK expression levels are not necessarily the main reason for the induction of the development of NAFLD [6,7]. On the other hand, restoration of AMPK activity does attenuate or reverse hepatic ste atosis [8].…”

Section: Introductionmentioning

confidence: 99%

Dapagliflozin Presented Nonalcoholic Fatty Liver Through Metabolite Extraction and AMPK/NLRP3 Signaling Pathway

Deng

Song

2022

Horm Metab Res

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In recent years, the incidence rate of nonalcoholic fatty liver disease (NAFLD) has been increasing year by year. The experiments conducted on rat elucidated the effect and underlying mechanism of dapagliflozin in NAFLD. Sprague Dawley rats were fed with HFD (Fat accounts for 52%, carbohydrate 34% and protein 14%) for 12 weeks as NAFLD model. Dapagliflozin presented NAFLD in rat model. Dapagliflozin reduced oxidative stress and inflammation in rat model of NAFLD. Dapagliflozin reduced oxidative stress and inflammation in vitro model of NAFLD. Dapagliflozin in a model of NAFLD metabolized into histamine H1 receptor, caffeine metabolism, mannose type O-glycan biosynthesis, choline metabolism in cancer, tryptophan metabolism, and glycerophospholipid metabolism. Dapagliflozin induced AMPK/NLRP3 signaling pathway. The regulation of AMPK/NLRP3 signaling pathway affected the effects of dapagliflozin on nonalcoholic fatty liver. In summary, dapagliflozin plays a preventative role in NAFLD through metabolite extraction, the inhibition of oxidative stress, and inflammation by AMPK/NLRP3 signaling pathway. Dapagliflozin may be a potential therapeutic agent for oxidative stress and inflammation in model of NAFLD.

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Aurantio-Obtusin Attenuates Non-Alcoholic Fatty Liver Disease Through AMPK-Mediated Autophagy and Fatty Acid Oxidation Pathways

Cited by 22 publications

References 47 publications

Lactobacillus plantarum ZJUIDS14 alleviates non-alcoholic fatty liver disease in mice in association with modulation in the gut microbiota

Lactobacillus plantarum ZJUIDS14 alleviates non-alcoholic fatty liver disease in mice in association with modulation in the gut microbiota

The Overlooked Transformation Mechanisms of VLCFAs: Peroxisomal β-Oxidation

Dapagliflozin Presented Nonalcoholic Fatty Liver Through Metabolite Extraction and AMPK/NLRP3 Signaling Pathway

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