ArticleNutrients2016
Platycodon grandiflorus Root Extract Attenuates Body Fat Mass, Hepatic Steatosis and Insulin Resistance through the Interplay between the Liver and Adipose Tissue.
Article in Nutrients, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
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- Estrogen-Related Receptor α: A Key Transcription Factor in the Regulation of Energy Metabolism at an Organismic Level and a Target of the ABA/LANCL Hormone Receptor System.International journal of molecular sciences · 2024Review
- Revealing Molecular Mechanisms of the Bioactive Saponins from Edible Root ofPlants (Basel, Switzerland) · 2024Article
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- Biological Role and Related Natural Products of SIRT1 in Nonalcoholic Fatty Liver.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Review
- The evolving view of thermogenic fat and its implications in cancer and metabolic diseases.Signal transduction and targeted therapy · 2022Review
- Transcriptome analysis identifies putative genes involved in triterpenoid biosynthesis in Platycodon grandiflorus.Planta · 2021Article
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- Mitophagy in Hepatic Insulin Resistance: Therapeutic Potential and Concerns.Frontiers in pharmacology · 2019Review
- Therapeutic Mechanisms of Herbal Medicines Against Insulin Resistance: A Review.Frontiers in pharmacology · 2019Review
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Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Platycodon grandiflorus root, a Korean medicinal food, is well known to have beneficial effects on obesity and diabetes. In this study, we demonstrated the metabolic effects of P. grandiflorus root ethanol extract (PGE), which is rich in platycodins, on diet-induced obesity. C57BL/6J mice (four-week-old males) were fed a normal diet (16.58% of kilocalories from fat), high-fat diet (HFD, 60% of kilocalories from fat), and HFD supplemented with 5% (w/w) PGE. In the HFD-fed mice, PGE markedly suppressed the body weight gain and white fat mass to normal control level, with simultaneous increase in the expression of thermogenic genes (such as SIRT1, PPARα, PGC1α, and UCP1), that accompanied changes in fatty acid oxidation (FAO) and energy expenditure. In addition, PGE improved insulin sensitivity through activation of the PPARγ expression, which upregulates adiponectin while decreasing leptin gene expression in adipocytes. Furthermore, PGE improved hepatic steatosis by suppressing hepatic lipogenesis while increasing expression of FAO-associated genes such as PGC1α. PGE normalized body fat and body weight, which is likely associated with the increased energy expenditure and thermogenic gene expression. PGE can protect from HFD-induced insulin resistance, and hepatic steatosis by controlling lipid and glucose metabolism.
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