Ginsenosides Rg1 regulate lipid metabolism and temperature adaptation in Caenorhabditis elegans

Shi, Hao; Zhao, Jianlong; Li, Yiwen; Li, Junjie; Li, Yunjia; Zhang, Jia; Qiu, Zhantu; Wu, Chaofeng; Qin, Mengchen; Liu, Chang; Zeng, Zhiyun; Zhang, Chao; Gao, Lei

doi:10.1016/j.jgr.2022.11.005

Cited by 2 publications

(1 citation statement)

References 39 publications

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“…Moreover, the side effects of the long-term prescription of approved anti-obesity medicines, such as gastro-intestinal disturbances, as well as insufficient efficacy encourage the development of novel approaches for obesity management [2,9]. As natural products are widely-accepted as safe, the identification of plant-based compounds that regulate energy and lipid metabolism offers a promising perspective [10][11][12][13]. Plant secondary metabolites may help restore dysregulated metabolic signaling pathways in obese patients through various mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Maackiain Mimics Caloric Restriction through aak-2-Mediated Lipid Reduction in Caenorhabditis elegans

Mladenova,

Todorova,

Savova

et al. 2023

IJMS

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Obesity prevalence is becoming a serious global health and economic issue and is a major risk factor for concomitant diseases that worsen the quality and duration of life. Therefore, the urgency of the development of novel therapies is of a particular importance. A previous study of ours revealed that the natural pterocarpan, maackiain (MACK), significantly inhibits adipogenic differentiation in human adipocytes through a peroxisome proliferator-activated receptor gamma (PPARγ)-dependent mechanism. Considering the observed anti-adipogenic potential of MACK, we aimed to further elucidate the molecular mechanisms that drive its biological activity in a Caenorhabditis elegans obesity model. Therefore, in the current study, the anti-obesogenic effect of MACK (25, 50, and 100 μM) was compared to orlistat (ORST, 12 μM) as a reference drug. Additionally, the hybrid combination between the ORST (12 μM) and MACK (100 μM) was assessed for suspected synergistic interaction. Mechanistically, the observed anti-obesogenic effect of MACK was mediated through the upregulation of the key metabolic regulators, namely, the nuclear hormone receptor 49 (nhr-49) that is a functional homologue of the mammalian PPARs and the AMP-activated protein kinase (aak-2/AMPK) in C. elegans. Collectively, our investigation indicates that MACK has the potential to limit lipid accumulation and control obesity that deserves future developments.

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