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Ginsenoside Rb1 Induces Beta 3 Adrenergic Receptor-Dependent Lipolysis and Thermogenesis in 3T3-L1 Adipocytes and db/db Mice.

ABSTRACT: Obesity is constantly rising into a major health threat worldwide. Activation of brown-like transdifferentiation of white adipocytes (browning) has been proposed as a promising molecular target for obesity treatment. In this study, we investigated the effect of ginsenoside Rb1 (Rb1), a saponin derived from Panax ginseng Meyer, on browning. We used 3T3-L1 murine adipocytes and leptin receptor mutated db/db mice. The lipid accumulation, AMP-activated protein kinase alpha (AMPK?)-related pathways, lipolytic and thermogenic factors were measured after Rb treatment in 3T3-L1 adipocytes. Body weight change and lipolysis-thermogenesis factors were investigated in Rb1-treated db/db mice. Beta 3 adrenergic receptor activation (?3AR) changes were measured in Rb1-treated 3T3-L1 cells with or without ?3AR inhibitor L748337 co-treatment. As a result, Rb1 treatment decreased lipid droplet size in 3T3-L1 adipocytes. Rb1 also induced phosphorylations of AMPK? pathway and sirtuins. Moreover, lipases and thermogenic factors such as uncoupling protein 1 were increased by Rb1 treatment. Through these results, we could expect that the non-shivering thermogenesis program can be induced by Rb1. In db/db mice, 6-week injection of Rb1 resulted in decreased inguinal white adipose tissue (iWAT) weight associated with shrunken lipid droplets and increased lipolysis and thermogenesis. The thermogenic effect of Rb1 was possibly due to ?3AR, as L748337 pre-treatment abolished the effect of Rb1. In conclusion, we suggest Rb1 as a potential lipolytic and thermogenic therapeutic agent which can be used for obesity treatment.

SUBMITTER: Lim S

PROVIDER: S-EPMC6803469 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Publications

Ginsenoside Rb1 Induces Beta 3 Adrenergic Receptor-Dependent Lipolysis and Thermogenesis in 3T3-L1 Adipocytes and <i>db/db</i> Mice.

Lim Seona S Park Jinbong J Um Jae-Young JY

Frontiers in pharmacology 20191015

Obesity is constantly rising into a major health threat worldwide. Activation of brown-like transdifferentiation of white adipocytes (browning) has been proposed as a promising molecular target for obesity treatment. In this study, we investigated the effect of ginsenoside Rb1 (Rb1), a saponin derived from <i>Panax ginseng</i> Meyer, on browning. We used 3T3-L1 murine adipocytes and leptin receptor mutated db/db mice. The lipid accumulation, AMP-activated protein kinase alpha (AMPKα)-related pat ...[more]

PMID: 31680950

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Project description:In obesity, high levels of tumor necrosis factor ? (TNF?) stimulate lipolysis in adipocytes, leading to hyperlipidemia and insulin resistance. Thiazolidinediones (TZDs), the insulin-sensitizing drugs, antagonize TNF?-induced lipolysis in adipocytes, thereby increasing insulin sensitivity in diabetes patients. The cellular target of TZDs is peroxisome proliferator-activated receptor ? (PPAR?), a nuclear receptor that controls many adipocyte functions. As a transcription factor, PPAR? is closely modulated by coregulators, which include coactivators and corepressors. Previous studies have revealed that in macrophages, the insulin-sensitizing effect of PPAR? may involve suppression of proinflammatory gene expression by recruiting the corepressor complex that contains corepressors and histone deacetylases (HDACs). Therefore, we investigated whether the corepressor complex is involved in TZD-mediated suppression of TNF?-induced lipolysis in 3T3-L1 adipocytes. Trichostatin A (TSA), a pan HDAC inhibitor (HDACI) that inhibits class I and II HDACs, was used to examine the involvement of HDACs in the actions of TZDs. TSA alone increased basal lipolysis and attenuated TZD-mediated suppression of TNF?-induced lipolysis. Increased basal lipolysis may in part result from class I HDAC inhibition because selective class I HDACI treatment had similar results. However, attenuation of TZD-mediated TNF? antagonism may be specific to TSA and related hydroxamate-based HDACI rather than to HDAC inhibition. Consistently, corepressor depletion did not affect TZD-mediated suppression. Interestingly, TSA treatment greatly reduced PPAR? levels in differentiated adipocytes. Finally, extracellular signal-related kinase 1/2 (ERK1/2) mediated TNF?-induced lipolysis, and TZDs suppressed TNF?-induced ERK phosphorylation. We determined that TSA increased basal ERK phosphorylation, and attenuated TZD-mediated suppression of TNF?-induced ERK phosphorylation, consistent with TSA's effects on lipolysis. These studies suggest that TSA, through down-regulating PPAR?, attenuates TZD-mediated suppression of TNF?-induced ERK phosphorylation and lipolysis in adipocytes.

Dataset Information

Ginsenoside Rb1 Induces Beta 3 Adrenergic Receptor-Dependent Lipolysis and Thermogenesis in 3T3-L1 Adipocytes and db/db Mice.

Publications

Ginsenoside Rb1 Induces Beta 3 Adrenergic Receptor-Dependent Lipolysis and Thermogenesis in 3T3-L1 Adipocytes and <i>db/db</i> Mice.

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