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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

Effects of dietary PGE on body weight gain, plasma lipid profiles, insulin resistance, and glucose tolerance via modulating hepatic glucose-regulating enzyme activities in HFD-fed C57BL/6J mice. The data are the mean ± SEM (n = 10). (A) Changes in the body weight, food intake, and food efficiency ratio (FER); (B) levels of plasma total, HDL, and non-HDL cholesterol, AI, TG, FFA, Apo A-1, and Apo B; (C) levels of plasma resistin, leptin, TNF-α, and PAI-1; (D) blood glucose levels after 12 h of fasting; (E) plasma insulin and glucose levels after 12 h of fasting and the HOMA-IR calculated using the fasting blood glucose and insulin levels; (F) glucose tolerance; and (G) activities of the glucose-regulating enzymes G6Pase and PEPCK. ND, mice fed a normal diet; HFD, mice fed a high-fat diet (HFD) alone; PGE, Platycodon grandiflorus root extract (5%, w/w)-treated HFD-fed mice. B.W., body weight, AI, atherogenic index, ((Total-C)-(HDL-C))/HDL-C.
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nutrients-08-00532-f001: Effects of dietary PGE on body weight gain, plasma lipid profiles, insulin resistance, and glucose tolerance via modulating hepatic glucose-regulating enzyme activities in HFD-fed C57BL/6J mice. The data are the mean ± SEM (n = 10). (A) Changes in the body weight, food intake, and food efficiency ratio (FER); (B) levels of plasma total, HDL, and non-HDL cholesterol, AI, TG, FFA, Apo A-1, and Apo B; (C) levels of plasma resistin, leptin, TNF-α, and PAI-1; (D) blood glucose levels after 12 h of fasting; (E) plasma insulin and glucose levels after 12 h of fasting and the HOMA-IR calculated using the fasting blood glucose and insulin levels; (F) glucose tolerance; and (G) activities of the glucose-regulating enzymes G6Pase and PEPCK. ND, mice fed a normal diet; HFD, mice fed a high-fat diet (HFD) alone; PGE, Platycodon grandiflorus root extract (5%, w/w)-treated HFD-fed mice. B.W., body weight, AI, atherogenic index, ((Total-C)-(HDL-C))/HDL-C.

Mentions: PGE significantly suppressed the body weight gain from the first week of high-fat feeding and decreased the food efficiency ratio, with no difference in food intake (Figure 1A). Interestingly, the addition of PGE led to a significant reduction of body weight compared to that in the HFD group, bringing it to the level similar to that in the ND group. PGE significantly decreased not only the total cholesterol (TC) and non-HDL cholesterol levels but also the apolipoprotein (Apo) B levels compared to those in the HFD group. The levels of plasma triglycerides (TG), and FFA were also markedly decreased by the PGE treatment compared to those in the HFD group (Figure 1B). Similar to the results for plasma lipid profiles, PGE significantly lowered the plasma adipokine levels, such as resistin, leptin, TNF-α, and plasminogen activator inhibitor-1 (PAI-1) levels (Figure 1C).


Platycodon grandiflorus Root Extract Attenuates Body Fat Mass, Hepatic Steatosis and Insulin Resistance through the Interplay between the Liver and Adipose Tissue
Effects of dietary PGE on body weight gain, plasma lipid profiles, insulin resistance, and glucose tolerance via modulating hepatic glucose-regulating enzyme activities in HFD-fed C57BL/6J mice. The data are the mean ± SEM (n = 10). (A) Changes in the body weight, food intake, and food efficiency ratio (FER); (B) levels of plasma total, HDL, and non-HDL cholesterol, AI, TG, FFA, Apo A-1, and Apo B; (C) levels of plasma resistin, leptin, TNF-α, and PAI-1; (D) blood glucose levels after 12 h of fasting; (E) plasma insulin and glucose levels after 12 h of fasting and the HOMA-IR calculated using the fasting blood glucose and insulin levels; (F) glucose tolerance; and (G) activities of the glucose-regulating enzymes G6Pase and PEPCK. ND, mice fed a normal diet; HFD, mice fed a high-fat diet (HFD) alone; PGE, Platycodon grandiflorus root extract (5%, w/w)-treated HFD-fed mice. B.W., body weight, AI, atherogenic index, ((Total-C)-(HDL-C))/HDL-C.
© Copyright Policy
Related In: Results  -  Collection

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

nutrients-08-00532-f001: Effects of dietary PGE on body weight gain, plasma lipid profiles, insulin resistance, and glucose tolerance via modulating hepatic glucose-regulating enzyme activities in HFD-fed C57BL/6J mice. The data are the mean ± SEM (n = 10). (A) Changes in the body weight, food intake, and food efficiency ratio (FER); (B) levels of plasma total, HDL, and non-HDL cholesterol, AI, TG, FFA, Apo A-1, and Apo B; (C) levels of plasma resistin, leptin, TNF-α, and PAI-1; (D) blood glucose levels after 12 h of fasting; (E) plasma insulin and glucose levels after 12 h of fasting and the HOMA-IR calculated using the fasting blood glucose and insulin levels; (F) glucose tolerance; and (G) activities of the glucose-regulating enzymes G6Pase and PEPCK. ND, mice fed a normal diet; HFD, mice fed a high-fat diet (HFD) alone; PGE, Platycodon grandiflorus root extract (5%, w/w)-treated HFD-fed mice. B.W., body weight, AI, atherogenic index, ((Total-C)-(HDL-C))/HDL-C.
Mentions: PGE significantly suppressed the body weight gain from the first week of high-fat feeding and decreased the food efficiency ratio, with no difference in food intake (Figure 1A). Interestingly, the addition of PGE led to a significant reduction of body weight compared to that in the HFD group, bringing it to the level similar to that in the ND group. PGE significantly decreased not only the total cholesterol (TC) and non-HDL cholesterol levels but also the apolipoprotein (Apo) B levels compared to those in the HFD group. The levels of plasma triglycerides (TG), and FFA were also markedly decreased by the PGE treatment compared to those in the HFD group (Figure 1B). Similar to the results for plasma lipid profiles, PGE significantly lowered the plasma adipokine levels, such as resistin, leptin, TNF-α, and plasminogen activator inhibitor-1 (PAI-1) levels (Figure 1C).

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