Regulation of Mitochondrial Function by Natural Products for the Treatment of Metabolic Associated Fatty Liver Disease

Shi, Tingting; Yu, Liping; Zhuang, Ran; Xi, Jianjun; He, Ruoyu; Shao, Yi; Huang, Jinsong; Liu, Shourong; Yang, Xiao‐Ke

doi:10.1155/2021/5527315

Cited by 6 publications

(3 citation statements)

References 39 publications

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“…Furthermore, recent studies indicate that mitochondrial regulators/nutrients from natural products can remedy mitochondrial dysfunction mediated by MAFLD [ 35 , 36 ]. Meanwhile, a number of researches nowadays are developing innovative drugs for the prevention and treatment of fatty liver diseases based on mitochondrial dysfunction [ 37 ]. The role of mitochondria as the metabolic center of cells in regulating macrophage function has been gradually revealed [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

The Imbalance of Mitochondrial Homeostasis of Peripheral Blood-Derived Macrophages Mediated by MAFLD May Impair the Walking Ability of Elderly Patients with Osteopenia

Wang

Liu

et al. 2022

Oxidative Medicine and Cellular Longevity

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Introduction. Many Asian cohort studies have shown that nonalcoholic fatty liver disease (NAFLD), now renamed as metabolic dysfunction-associated fatty liver disease (MAFLD), increases the risk of osteoporosis, yet the effect of MAFLD on elderly patients with osteopenia (OPe) has not been reported. Objective. This study aimed to explore the influence of MAFLD on the function of macrophages in patients with OPe. Methods. A total of 107 elderly OPe patients with or without MAFLD who visited the Huadong Hospital Affiliated to Fudan University (Shanghai, China) between January 1st, 2021, and September 30th, 2021, were evaluated for an interviewer-assisted questionnaire, as well as clinical and biological assessments. Results. Comparing two groups of elderly patients with the same bone mass level, we found that the six-minute walking distance ( P = 0.012 ) and short physical performance battery (SPPB) score ( P = 0.0029 ) of the elderly OPe patients with MAFLD are worse than those in OPe patients without MAFLD. Our results confirmed that the mitochondrial reactive oxygen species (mtROS) in peripheral blood of OPe patients with MAFLD was significantly higher than those without. We also observed the mitochondrial metabolism level of peripheral blood-derived macrophages in the included patients and peripheral blood macrophages in patients with MAFLD with more unbalanced mitochondrial dynamics of macrophages, more weakened mitochondrial respiratory capacity, and greater mitochondrial microstructure damage, when compared with the elderly patients without MAFLD. Conclusions. To conclude, our data revealed that MAFLD itself may aggravate the inflammatory state in elderly OPe people due to mitochondrial homeostasis imbalance of peripheral blood macrophages. Damaged monocyte-macrophages might trigger attenuation of the walking ability of OPe patients.

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Section: Discussionmentioning

confidence: 99%

The Imbalance of Mitochondrial Homeostasis of Peripheral Blood-Derived Macrophages Mediated by MAFLD May Impair the Walking Ability of Elderly Patients with Osteopenia

Wang

Liu

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…In addition to the improvement of hepatic fat accumulation and metabolism, exercise can also regulate the function of liver resident macrophages to modulate liver inflammation and fibrosis [ 82 ] . In addition, exercise can improve mitochondrial function to enhance aerobic metabolism [ 83 ] . However, exercise can also directly cause abnormal liver function tests in healthy young adults [ 84 ] .…”

Section: Factors Regulate the Change Of Gut Microbiota And Their Meta...mentioning

confidence: 99%

Gut microbiota and metabolite interface-mediated hepatic inflammation

Yang,

Massad,

Kimchi

et al. 2024

Immunometabolism

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Immunologic and metabolic signals regulated by gut microbiota and relevant metabolites mediate bidirectional interaction between the gut and liver. Gut microbiota dysbiosis, due to diet, lifestyle, bile acids, and genetic and environmental factors, can advance the progression of chronic liver disease. Commensal gut bacteria have both pro- and anti-inflammatory effects depending on their species and relative abundance in the intestine. Components and metabolites derived from gut microbiota–diet interaction can regulate hepatic innate and adaptive immune cells, as well as liver parenchymal cells, significantly impacting liver inflammation. In this mini review, recent findings of specific bacterial species and metabolites with functions in regulating liver inflammation are first reviewed. In addition, socioeconomic and environmental factors, hormones, and genetics that shape the profile of gut microbiota and microbial metabolites and components with the function of priming or dampening liver inflammation are discussed. Finally, current clinical trials evaluating the factors that manipulate gut microbiota to treat liver inflammation and chronic liver disease are reviewed. Overall, the discussion of microbial and metabolic mediators contributing to liver inflammation will help direct our future studies on liver disease.

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“…Inhibition of lipid uptake can be a target for the prevention and control of NAFLD. Many natural products have been reported to exert efficacy in alleviating NAFLD by modulating lipid metabolism disorder . Therefore, searching for active molecules against NAFLD from natural products is an attractive therapeutic strategy.…”

Section: Introductionmentioning

confidence: 99%

Millet Bran Protein Hydrolysate Displays the Anti-non-alcoholic Fatty Liver Disease Effect via Activating Peroxisome Proliferator-Activated Receptor γ to Restrain Fatty Acid Uptake

Shan

Zhou

Yin

et al. 2023

J. Agric. Food Chem.

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Non-alcoholic fatty liver disease (NAFLD) is a serious health problem worldwide. Impeding fatty acid uptake may be an attractive therapeutic strategy for NAFLD. In the current study, we found that millet bran protein hydrolysate (MBPH) prepared by in vitro gastrointestinal bionic digestion exhibits the potential of anti-NAFLD in vitro and in vivo, characterized by the alleviation of hepatic steatosis and the reduction of lipid accumulation. Further, MBPH significantly decreased the expression levels of fatty acid uptake related genes (FABP1, FABP2, FABP4, CD36, and CPT-1α) of liver tissue in a NAFLD mice model through activating peroxisome proliferator-activated receptor γ (PPARγ) and efficiently restrained the fatty acid uptake of liver tissue, thus exerting anti-NAFLD activity. As expected, the anti-NAFLD effect induced by MBPH, characterized by the alleviation of hepatic vacuolar degeneration, hepatic steatosis, and fibrosis, was effectively abrogated with PPARγ inhibitor (GW9662) treatment. These results indicate that the retardant of fatty acid uptake induced by PPARγ activation may be the critical factor for the anti-NAFLD effect of MBPH. Collectively, MBPH has the potential as a next-generation dietary supplementation for the prevention and treatment of NAFLD.

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Regulation of Mitochondrial Function by Natural Products for the Treatment of Metabolic Associated Fatty Liver Disease

Cited by 6 publications

References 39 publications

The Imbalance of Mitochondrial Homeostasis of Peripheral Blood-Derived Macrophages Mediated by MAFLD May Impair the Walking Ability of Elderly Patients with Osteopenia

The Imbalance of Mitochondrial Homeostasis of Peripheral Blood-Derived Macrophages Mediated by MAFLD May Impair the Walking Ability of Elderly Patients with Osteopenia

Gut microbiota and metabolite interface-mediated hepatic inflammation

Millet Bran Protein Hydrolysate Displays the Anti-non-alcoholic Fatty Liver Disease Effect via Activating Peroxisome Proliferator-Activated Receptor γ to Restrain Fatty Acid Uptake

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