Improvement and Mechanism of <i>Ganoderma lucidum</i> Polysaccharides and Its Flora Metabolites on Insulin Resistance in HepG2 Cells

LIU Shifeng; DONG Wenjing; YANG Lan; ZHOU Jiali; LIU Dongbo

doi:10.13386/j.issn1002-0306.2023020035

Volume 44 Issue 23

Nov. 2023

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Science and Technology of Food Industry > 2023 > 44(23): 314-321. > DOI: 10.13386/j.issn1002-0306.2023020035

LIU Shifeng, DONG Wenjing, YANG Lan, et al. Improvement and Mechanism of Ganoderma lucidum Polysaccharides and Its Flora Metabolites on Insulin Resistance in HepG2 Cells[J]. Science and Technology of Food Industry, 2023, 44(23): 314−321. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2023020035.

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Improvement and Mechanism of Ganoderma lucidum Polysaccharides and Its Flora Metabolites on Insulin Resistance in HepG2 Cells

LIU Shifeng^{1, 2,},
DONG Wenjing^{1, 2},
YANG Lan^{1, 2, 3},
ZHOU Jiali^{1, 2},
LIU Dongbo^{1, 2, ,}

1.
College of Horticulture and Landscape, Hunan Agricultural University, Changsha 410128, China
2.
State Key Laboratory of Subhealth Intervention Technology, Changsha 410128, China
3.
North Sichuan Medical College, Nanchong 637000, China

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Received Date: February 08, 2023
Available Online: October 03, 2023

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Abstract

Abstract

Objective: To investigate the effects of Ganoderma lucidum polysaccharides and its flora metabolites on the insulin resistance status of HepG2 cells and its mechanisms. Methods: Insulin resistant HepG2 (IR-HepG2) model was established with the combination of insulin (10⁻³µmol/L) and dexamethasone (10 µmol/L). The cytotoxicity of Ganoderma lucidum polysaccharides (GLP) and Ganoderma lucidum polysaccharide flora metabolite (GLP-F) was evaluated using the CCK-8 method. The effects of GLP and GLP-F on glucose consumption and glycogen synthesis in IR-HepG2 cells were evaluated using the glucose kit and glycogen kit methods. Western blot assay was used to detect the effects of GLP and GLP-F on the phosphorylation or expression of IRS-1, AKT, GSK-3β, GLUT2, and PEPCK, key proteins in the insulin signaling cascade in IR-HepG2 cells. Results: Both GLP and GLP-F significantly increased glucose uptake and glycogen synthesis in IR-HepG2 cells (P<0.05). GLP-F promoted glucose consumption in IR-HepG2 cells significantly more than GLP (P<0.05). Western blot experiments showed that both GLP and GLP-F promoted IR-HepG2 cells IRS-1, P-AKT, P-GSK-3β, GLUT2 protein expression and inhibited PEPCK protein expression, and the inhibitory utility of GLP-F on PEPCK was significantly higher than that of GLP (P<0.05). Conclusions: GLP and its metabolism by intestinal flora-mediated production of GLP-F have the same biological effect of alleviating hepatic insulin resistance, and GLP-F has a more significant effect than GLP in promoting glucose consumption in IR-HepG2 cells and inhibiting their gluconeogenic rate-limiting enzyme activity.

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