Gallic acid impairs fructose-driven de novo lipogenesis and ameliorates hepatic steatosis via AMPK-dependent suppression of SREBP-1/ACC/FASN cascade

Lu, Yuzhen; Zhang, Cong; Song, Yingying; Chen, Liang; Chen, Xin; Zheng, Guohua; Yang, Yuan; Cao, Peng; Qiu, Zhenpeng

doi:10.1016/j.ejphar.2022.175457

Cited by 13 publications

(6 citation statements)

References 26 publications

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“…In line with this conclusion, Fang et al [ 65 ] demonstrated that gallotannin derivatives from mango counteract adipogenesis by activating AMPK. In addition, Lu, et al showed that gallic acid reduced lipogenesis and improved liver steatosis by activating AMPK [ 66 ]. This effect could result by a direct interaction of gallic acid with AMPKα/β subunits, as evidenced by computational docking analysis [ 66 ].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, Lu, et al showed that gallic acid reduced lipogenesis and improved liver steatosis by activating AMPK [ 66 ]. This effect could result by a direct interaction of gallic acid with AMPKα/β subunits, as evidenced by computational docking analysis [ 66 ]. Finally, mangiferin, a polyphenol derived from Mangifera indica promotes browning of adipocytes by activating AMPK [ 67 ].…”

Section: Discussionmentioning

confidence: 99%

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Hypertrophy and ER Stress Induced by Palmitate Are Counteracted by Mango Peel and Seed Extracts in 3T3-L1 Adipocytes

Pratelli

Liberto

Carlisi

et al. 2023

IJMS

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A diet rich in saturated fatty acids (FAs) has been correlated with metabolic dysfunction and ROS increase in the adipose tissue of obese subjects. Thus, reducing hypertrophy and oxidative stress in adipose tissue can represent a strategy to counteract obesity and obesity-related diseases. In this context, the present study showed how the peel and seed extracts of mango (Mangifera indica L.) reduced lipotoxicity induced by high doses of sodium palmitate (PA) in differentiated 3T3-L1 adipocytes. Mango peel (MPE) and mango seed (MSE) extracts significantly lowered PA-induced fat accumulation by reducing lipid droplet (LDs) and triacylglycerol (TAGs) content in adipocytes. We showed that MPE and MSE activated hormone-sensitive lipase, the key enzyme of TAG degradation. In addition, mango extracts down-regulated the adipogenic transcription factor PPARγ as well as activated AMPK with the consequent inhibition of acetyl-CoA-carboxylase (ACC). Notably, PA increased endoplasmic reticulum (ER) stress markers GRP78, PERK and CHOP, as well as enhanced the reactive oxygen species (ROS) content in adipocytes. These effects were accompanied by a reduction in cell viability and the induction of apoptosis. Interestingly, MPE and MSE counteracted PA-induced lipotoxicity by reducing ER stress markers and ROS production. In addition, MPE and MSE increased the level of the anti-oxidant transcription factor Nrf2 and its targets MnSOD and HO-1. Collectively, these results suggest that the intake of mango extract-enriched foods in association with a correct lifestyle could exert beneficial effects to counteract obesity.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hypertrophy and ER Stress Induced by Palmitate Are Counteracted by Mango Peel and Seed Extracts in 3T3-L1 Adipocytes

Pratelli

Liberto

Carlisi

et al. 2023

IJMS

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“…Diosgenin, in addition to reducing fatty acid uptake, can also inhibit hepatic DNL by activating AMPK and downregulating SREBP1c, thereby alleviating MAFLD [269,271]. Gallic acid, an abundant polyphenolic compound found in vegetables and fruits, can ameliorate fructose-induced hepatic steatosis by inhibiting hepatic DNL through AMPK-dependent mechanisms [272]. A natural flavonoid, Baicalein, also alleviated MAFLD through a similar mechanism [273].…”

Section: Natural Products and Dnl In Mafldmentioning

confidence: 99%

Examining the Pathogenesis of MAFLD and the Medicinal Properties of Natural Products from a Metabolic Perspective

Fu,

Wang,

Qin

2024

Metabolites

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Metabolic-associated fatty liver disease (MAFLD), characterized primarily by hepatic steatosis, has become the most prevalent liver disease worldwide, affecting approximately two-fifths of the global population. The pathogenesis of MAFLD is extremely complex, and to date, there are no approved therapeutic drugs for clinical use. Considerable evidence indicates that various metabolic disorders play a pivotal role in the progression of MAFLD, including lipids, carbohydrates, amino acids, and micronutrients. In recent years, the medicinal properties of natural products have attracted widespread attention, and numerous studies have reported their efficacy in ameliorating metabolic disorders and subsequently alleviating MAFLD. This review aims to summarize the metabolic-associated pathological mechanisms of MAFLD, as well as the natural products that regulate metabolic pathways to alleviate MAFLD.

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“…Furthermore, an initial evaluation of ferulic acid's anticancer activity in HepG2 cells demonstrated its role in inhibiting tumor cell proliferation through inducing apoptosis and autophagy . High-fructose-induced hyperuricemia and NAFLD C1q /CTRP3(+)/ACL(-) (Elseweidy et al, 2022) Ferulic acid Cecal ligation and perforation (CLP)-induced and lipopolysaccharide (LPS)-induced ALI GSK-3β/CREB/ NF-κB(-) (Cao et al, 2021) Aflatoxin B1-induced liver damage CYP450(-)/Nrf2/GST(+) (Wang, He, et al, 2021) CCl4-induced hepatic fibrosis TGF-β1/ Smads(-) (Mu et al, 2018) HCHF-induced NASH ROCK/NF-κB(-) (Wei et al, 2021) HFD-induced NAFLD PPARα(+) (Luo et al, 2022) Chlorogenic acid CCl4-induced liver fibrosis and inflammation TLR4/MyD88/NF-κB(-) (Shi et al, 2013) ANIT-induced liver injury STAT3/NF-κB(-) (Tan et al, 2016) CCl4-induced liver injury NLRP3(-)/Nrf2(+) (Shi et al, 2018) HFD-induced NAFLD TLR4(-) (Shi et al, 2021) MCDD diet-induced NAFLD LPS-TLR4-MyD88(-) (Gu et al, 2023) MCD diet-induced NAFLD ECM/HSCs(-) (Miao et al, 2022) HCC cells Hep-G2 and Huh-7 NF-κB(-)/BBC3(+) (Jiang et al, 2021) Gallic acid aHSCs TRADD/RIP3(+) (Chang et al, 2015) HFD-induced NAFLD rats and palmitic acid (PA) and oleic acid (OA)-treated hepatocytes AMPK/ACC/PPARα(-) (J. Fructose-induced NAFLD AMPK/SREBP-1/ ACC/ FASN axis (-) (Lu et al, 2023)…”

Section: Ferulic Acidmentioning

confidence: 99%

“…A subsequent study indicated that gallic acid ameliorated HFD‐induced NAFLD by regulating lipid metabolism and repairing mitochondrial damage via the inhibition of AMPK/ACC/PPARα signaling (J. Zhang, Zhang, et al, 2023). In addition, similar to ellagic acid, gallic acid treatment was proved to reduce hepatic de novo fat production and thus relieved NASH via suppressing SREBP‐1/ ACC/ FASN axis mediated by AMPK signals (Lu et al, 2023).…”

Section: Mechanisms Of Polyphenolic Compounds Protect Against Hepatic...mentioning

confidence: 99%

Human diet‐derived polyphenolic compounds and hepatic diseases: From therapeutic mechanisms to clinical utilization

Hu,

Zhang,

Wei

et al. 2023

Phytotherapy Research

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This review focuses on the potential ameliorative effects of polyphenolic compounds derived from human diet on hepatic diseases. It discusses the molecular mechanisms and recent advancements in clinical applications. Edible polyphenols have been found to play a therapeutic role, particularly in liver injury, liver fibrosis, NAFLD/NASH, and HCC. In the regulation of liver injury, polyphenols exhibit anti‐inflammatory and antioxidant effects, primarily targeting the TGF‐β, NF‐κB/TLR4, PI3K/AKT, and Nrf2/HO‐1 signaling pathways. In the regulation of liver fibrosis, polyphenolic compounds effectively reverse the fibrotic process by inhibiting the activation of hepatic stellate cells (HSC). Furthermore, polyphenolic compounds show efficacy against NAFLD/NASH by inhibiting lipid oxidation and accumulation, mediated through the AMPK, SIRT, and PPARγ pathways. Moreover, several polyphenolic compounds exhibit anti‐HCC activity by suppressing tumor cell proliferation and metastasis. This inhibition primarily involves blocking Akt and Wnt signaling, as well as inhibiting the epithelial‐mesenchymal transition (EMT). Additionally, clinical trials and nutritional evidence support the notion that certain polyphenols can improve liver disease and associated metabolic disorders. However, further fundamental research and clinical trials are warranted to validate the efficacy of dietary polyphenols.

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Gallic acid impairs fructose-driven de novo lipogenesis and ameliorates hepatic steatosis via AMPK-dependent suppression of SREBP-1/ACC/FASN cascade

Cited by 13 publications

References 26 publications

Hypertrophy and ER Stress Induced by Palmitate Are Counteracted by Mango Peel and Seed Extracts in 3T3-L1 Adipocytes

Hypertrophy and ER Stress Induced by Palmitate Are Counteracted by Mango Peel and Seed Extracts in 3T3-L1 Adipocytes

Examining the Pathogenesis of MAFLD and the Medicinal Properties of Natural Products from a Metabolic Perspective

Human diet‐derived polyphenolic compounds and hepatic diseases: From therapeutic mechanisms to clinical utilization

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