Effect of Genistein on Cholesterol Metabolism‐Related Genes in HepG2 Cell

Lu, Rongrong; Zheng, Zicong; Yin, Yongqiang; Jiang, Zijian

doi:10.1111/1750-3841.14725

Cited by 16 publications

(11 citation statements)

References 55 publications

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“…By comparing the effects of GEN to E2, we elucidated that treatment with GEN could inhibit lipid accumulation, similar to the condition of having circulating E2 in vivo. Several other studies that used ovariectomized rats [12] or HepG2 cells without PA treatment [27,28,32,33] proved that GEN was able to regulate lipid metabolism in their respective experimental models, which was consistent with our results.…”

Section: Discussionsupporting

confidence: 92%

Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells

et al. 2021

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Genistein (GEN) has been shown to significantly inhibit hepatic triglyceride accretion triggered by estrogen deficiency. The main purpose of this in vitro study was to investigate the function and molecular mechanism of estrogen receptor β (ERβ) in regulating hepatic lipid metabolism induced by GEN. Different doses of GEN or GEN with an ERβ antagonist were treated with HepG2 cells. Results showed that 25 μM GEN significantly diminished triglyceride levels. Meanwhile, GEN downregulated the levels of genes and proteins involved in lipogenesis, such as sterol-regulatory element-binding protein-1c (SREBP-1c), fatty acid synthase (FASN), and stearoyl-coenzyme A desaturase 1 (SCD1), and upregulated the gene and protein levels of the regulation factors responsible for fatty acid β-oxidation, such as carnitine palmitoyltransferase 1α (CPT-1α) and peroxisome proliferator-activated receptor α (PPARα). Furthermore, 25 μM GEN reduced the levels of phosphorylation of protein kinase B (Akt) and mechanistic target of rapamycin (mTOR). Moreover, most of these effects from GEN were reverted by pretreatment with the antagonist of ERβ. In conclusion, GEN improved hepatic lipid metabolism by activating ERβ and further modulation of Akt/mTOR signals. The results provide novel aspects of the regulatory mechanism of ERβ on hepatic lipid metabolism and might help to profoundly understand the functions of food-derived phytoestrogens in preventing and treating hepatic steatosis in postmenopausal women.

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Section: Discussionsupporting

confidence: 92%

Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells

et al. 2021

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“…ABCA1 transcription can be regulated by obligate heterodimers of liver X receptors (LXRs) and retinoid X receptors (RXRs), bacterial endotoxins such as LPS and peroxisome proliferator-activated receptors (PPARs) [ 40 , 44 , 45 ]. LXR is a transcription factor for ABCA1 [ 46 ].…”

Section: Abc Transporter Membersmentioning

confidence: 99%

The impact of ATP-binding cassette transporters on metabolic diseases

Lü

2020

Nutr Metab (Lond)

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Currently, many people worldwide suffer from metabolic diseases caused by heredity and external factors, such as diet. One of the symptoms of metabolic diseases is abnormal lipid metabolism. ATP binding cassette (ABC) transporters are one of the largest transport protein superfamilies that exist in nearly all living organisms and are mainly located on lipid-processing cells. ABC transporters have been confirmed to be closely related to the pathogenesis of diseases such as metabolic diseases, cancer and Alzheimer’s disease based on their transport abilities. Notably, the capability to transport lipids makes ABC transporters critical in metabolic diseases. In addition, gene polymorphism in ABC transporters has been reported to be a risk factor for metabolic diseases, and it has been reported that relevant miRNAs have significant roles in regulating ABC transporters. In this review, we integrate recent studies to examine the roles of ABC transporters in metabolic diseases and aim to build a network with ABC transporters as the core, linking their transport abilities with metabolic and other diseases.

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“…In particular, genistein increased the expression of UCP-1 and stimulated or promoted the browning of white adipocytes. Another study showed that in the liver cell line HepG2, genistein (≥1 μM) increased the intracellular cholesterol levels by inhibiting the PPARγ/LXRα/ABCA1 pathway via the SREBP-2/LDLR/HMGCR pathway [ 125 ]. Hence, the effect of genistein on the intracellular cholesterol level effectively reduced the plasma cholesterol levels and helped prevent atherosclerosis [ 125 ].…”

Section: Effects Of Isoflavones On Metabolic Syndrome and Its Constituent Diseasesmentioning

confidence: 99%

“…Another study showed that in the liver cell line HepG2, genistein (≥1 μM) increased the intracellular cholesterol levels by inhibiting the PPARγ/LXRα/ABCA1 pathway via the SREBP-2/LDLR/HMGCR pathway [ 125 ]. Hence, the effect of genistein on the intracellular cholesterol level effectively reduced the plasma cholesterol levels and helped prevent atherosclerosis [ 125 ]. Mouse muscle C2C12 cells were used to investigate the effect of daidzein on fatty acid metabolism in muscle cells [ 126 ].…”

Section: Effects Of Isoflavones On Metabolic Syndrome and Its Constituent Diseasesmentioning

confidence: 99%

Potential Effects of Soy Isoflavones on the Prevention of Metabolic Syndrome

Yamagata

Yamori

2021

Molecules

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Isoflavones are polyphenols primarily contained in soybean. As phytoestrogens, isoflavones exert beneficial effects on various chronic diseases. Metabolic syndrome increases the risk of death due to arteriosclerosis in individuals with various pathological conditions, including obesity, hypertension, hyperglycemia, and dyslipidemia. Although the health benefits of soybean-derived isoflavones are widely known, their beneficial effects on the pathogenesis of metabolic syndrome are incompletely understood. This review aims to describe the association between soybean-derived isoflavone intake and the risk of metabolic syndrome development. We reviewed studies on soy isoflavones, particularly daidzein and genistein, and metabolic syndrome, using PubMed, ScienceDirect, and Web of Science. We describe the pathological characteristics of metabolic syndrome, including those contributing to multiple pathological conditions. Furthermore, we summarize the effects of soybean-derived daidzein and genistein on metabolic syndrome reported in human epidemiological studies and experiments using in vitro and in vivo models. In particular, we emphasize the role of soy isoflavones in metabolic syndrome-induced cardiovascular diseases. In conclusion, this review focuses on the potential of soy isoflavones to prevent metabolic syndrome by influencing the onset of hypertension, hyperglycemia, dyslipidemia, and arteriosclerosis and discusses the anti-inflammatory effects of isoflavones.

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Effect of Genistein on Cholesterol Metabolism‐Related Genes in HepG2 Cell

Cited by 16 publications

References 55 publications

Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells

Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells

The impact of ATP-binding cassette transporters on metabolic diseases

Potential Effects of Soy Isoflavones on the Prevention of Metabolic Syndrome

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