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

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....

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Autores principales:	Hong Qin, Ziyu Song, Horia Shaukat, Wenya Zheng
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	genistein hepatic lipid metabolism estrogen receptor β Akt mTOR Nutrition. Foods and food supply TX341-641
Acceso en línea:	https://doaj.org/article/5a36b3571a3140cfa5eb879278a5daf5
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spelling	oai:doaj.org-article:5a36b3571a3140cfa5eb879278a5daf52021-11-25T18:36:07ZGenistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells10.3390/nu131140152072-6643https://doaj.org/article/5a36b3571a3140cfa5eb879278a5daf52021-11-01T00:00:00Zhttps://www.mdpi.com/2072-6643/13/11/4015https://doaj.org/toc/2072-6643Genistein (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.Hong QinZiyu SongHoria ShaukatWenya ZhengMDPI AGarticlegenisteinhepatic lipid metabolismestrogen receptor βAktmTORNutrition. Foods and food supplyTX341-641ENNutrients, Vol 13, Iss 4015, p 4015 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	genistein hepatic lipid metabolism estrogen receptor β Akt mTOR Nutrition. Foods and food supply TX341-641
spellingShingle	genistein hepatic lipid metabolism estrogen receptor β Akt mTOR Nutrition. Foods and food supply TX341-641 Hong Qin Ziyu Song Horia Shaukat Wenya Zheng Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells
description	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.
format	article
author	Hong Qin Ziyu Song Horia Shaukat Wenya Zheng
author_facet	Hong Qin Ziyu Song Horia Shaukat Wenya Zheng
author_sort	Hong Qin
title	Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells
title_short	Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells
title_full	Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells
title_fullStr	Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells
title_full_unstemmed	Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells
title_sort	genistein regulates lipid metabolism via estrogen receptor β and its downstream signal akt/mtor in hepg2 cells
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/5a36b3571a3140cfa5eb879278a5daf5
work_keys_str_mv	AT hongqin genisteinregulateslipidmetabolismviaestrogenreceptorbanditsdownstreamsignalaktmtorinhepg2cells AT ziyusong genisteinregulateslipidmetabolismviaestrogenreceptorbanditsdownstreamsignalaktmtorinhepg2cells AT horiashaukat genisteinregulateslipidmetabolismviaestrogenreceptorbanditsdownstreamsignalaktmtorinhepg2cells AT wenyazheng genisteinregulateslipidmetabolismviaestrogenreceptorbanditsdownstreamsignalaktmtorinhepg2cells
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Genistein Regulates Lipid Metabolism via Estrogen Receptor β and Its Downstream Signal Akt/mTOR in HepG2 Cells

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