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Platycodon grandiflorus Root Extract Attenuates Body Fat Mass, Hepatic Steatosis and Insulin Resistance through the Interplay between the Liver and Adipose Tissue

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Related in: MedlinePlus

Proposed mechanism for PGE regarding anti-obesity effects. Schematic representation of the role of PGE in amelioration of obesity. PGE can contribute to browning of WAT in diet-induced obese mice through increasing fatty acid oxidation in mitochondria, which promotes energy expenditure. In addition, PPARγ activation by PGE controls adipokines, specifically the insulin-sensitizing hormones adiponectin and leptin. In the liver, PGE downregulates the mRNA expression of lipogenesis and cholesterol synthesis transcription factors, SREBP1 and SREBP2, thereby reducing hepatic steatosis and insulin resistance. PPARγ, peroxisome proliferator-activated receptor γ; SREBP1a, -1c, and -2, sterol regulatory element-binding proteins 1a, 1c, and 2; FAS, fatty acid synthase; ACC, acetyl-CoA carboxylase; SCD1, stearoyl-CoA desaturase; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase; ACAT, acetyl-CoA acetyltransferase; SIRT1, sirtuin 1; PPARα, peroxisome proliferator-activated receptor α; PGC1α, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; UCP1, uncoupling protein 1; TNF-α, tumor necrosis factor-α; CPT2, carnitine palmitoyltransferase 2.
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nutrients-08-00532-f004: Proposed mechanism for PGE regarding anti-obesity effects. Schematic representation of the role of PGE in amelioration of obesity. PGE can contribute to browning of WAT in diet-induced obese mice through increasing fatty acid oxidation in mitochondria, which promotes energy expenditure. In addition, PPARγ activation by PGE controls adipokines, specifically the insulin-sensitizing hormones adiponectin and leptin. In the liver, PGE downregulates the mRNA expression of lipogenesis and cholesterol synthesis transcription factors, SREBP1 and SREBP2, thereby reducing hepatic steatosis and insulin resistance. PPARγ, peroxisome proliferator-activated receptor γ; SREBP1a, -1c, and -2, sterol regulatory element-binding proteins 1a, 1c, and 2; FAS, fatty acid synthase; ACC, acetyl-CoA carboxylase; SCD1, stearoyl-CoA desaturase; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase; ACAT, acetyl-CoA acetyltransferase; SIRT1, sirtuin 1; PPARα, peroxisome proliferator-activated receptor α; PGC1α, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; UCP1, uncoupling protein 1; TNF-α, tumor necrosis factor-α; CPT2, carnitine palmitoyltransferase 2.

Mentions: This study demonstrated that the PGE treatment normalized the body weight and body fat mass in the HFD-fed mice by increasing FAO. This partly changed the levels of thermogenesis-related genes such as UCP1 as well as PPARα, PGC1α, and SIRT1 and thus could promote BAT-like features in WAT, as well as enhance energy expenditure. Furthermore, reducing the WAT mass by the PGE treatment enhanced the susceptibility to developing hepatic steatosis and insulin resistance. Figure 4 illustrates the possible mechanisms of the PGE effects for antiobesity. Taken together, PGE can suppress diet-induced obesity and modulate obesity-associated metabolic disorders.


Platycodon grandiflorus Root Extract Attenuates Body Fat Mass, Hepatic Steatosis and Insulin Resistance through the Interplay between the Liver and Adipose Tissue
Proposed mechanism for PGE regarding anti-obesity effects. Schematic representation of the role of PGE in amelioration of obesity. PGE can contribute to browning of WAT in diet-induced obese mice through increasing fatty acid oxidation in mitochondria, which promotes energy expenditure. In addition, PPARγ activation by PGE controls adipokines, specifically the insulin-sensitizing hormones adiponectin and leptin. In the liver, PGE downregulates the mRNA expression of lipogenesis and cholesterol synthesis transcription factors, SREBP1 and SREBP2, thereby reducing hepatic steatosis and insulin resistance. PPARγ, peroxisome proliferator-activated receptor γ; SREBP1a, -1c, and -2, sterol regulatory element-binding proteins 1a, 1c, and 2; FAS, fatty acid synthase; ACC, acetyl-CoA carboxylase; SCD1, stearoyl-CoA desaturase; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase; ACAT, acetyl-CoA acetyltransferase; SIRT1, sirtuin 1; PPARα, peroxisome proliferator-activated receptor α; PGC1α, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; UCP1, uncoupling protein 1; TNF-α, tumor necrosis factor-α; CPT2, carnitine palmitoyltransferase 2.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037519&req=5

nutrients-08-00532-f004: Proposed mechanism for PGE regarding anti-obesity effects. Schematic representation of the role of PGE in amelioration of obesity. PGE can contribute to browning of WAT in diet-induced obese mice through increasing fatty acid oxidation in mitochondria, which promotes energy expenditure. In addition, PPARγ activation by PGE controls adipokines, specifically the insulin-sensitizing hormones adiponectin and leptin. In the liver, PGE downregulates the mRNA expression of lipogenesis and cholesterol synthesis transcription factors, SREBP1 and SREBP2, thereby reducing hepatic steatosis and insulin resistance. PPARγ, peroxisome proliferator-activated receptor γ; SREBP1a, -1c, and -2, sterol regulatory element-binding proteins 1a, 1c, and 2; FAS, fatty acid synthase; ACC, acetyl-CoA carboxylase; SCD1, stearoyl-CoA desaturase; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase; ACAT, acetyl-CoA acetyltransferase; SIRT1, sirtuin 1; PPARα, peroxisome proliferator-activated receptor α; PGC1α, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; UCP1, uncoupling protein 1; TNF-α, tumor necrosis factor-α; CPT2, carnitine palmitoyltransferase 2.
Mentions: This study demonstrated that the PGE treatment normalized the body weight and body fat mass in the HFD-fed mice by increasing FAO. This partly changed the levels of thermogenesis-related genes such as UCP1 as well as PPARα, PGC1α, and SIRT1 and thus could promote BAT-like features in WAT, as well as enhance energy expenditure. Furthermore, reducing the WAT mass by the PGE treatment enhanced the susceptibility to developing hepatic steatosis and insulin resistance. Figure 4 illustrates the possible mechanisms of the PGE effects for antiobesity. Taken together, PGE can suppress diet-induced obesity and modulate obesity-associated metabolic disorders.

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Related in: MedlinePlus