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Effect of keishibukuryogan on genetic and dietary obesity models.

Gao F, Yokoyama S, Fujimoto M, Tsuneyama K, Saiki I, Shimada Y, Hayakawa Y - Evid Based Complement Alternat Med (2015)

Bottom Line: Obesity has been recognized as one of the most important risk factors for a variety of chronic diseases, such as diabetes, hypertension/cardiovascular diseases, steatosis/hepatitis, and cancer.Keishibukuryogan (KBG, Gui Zhi Fu Ling Wan in Chinese) is a traditional Chinese/Japanese (Kampo) medicine that has been known to improve blood circulation and is also known for its anti-inflammatory or scavenging effect.Importantly, we further found downregulation of genes involved in lipid metabolism in the KBG-treated liver, along with decreased liver TG and cholesterol level.

View Article: PubMed Central - PubMed

Affiliation: Division of Pathogenic Biochemistry, Institute of Natural Medicine, University of Toyama, Toyama 930-0194, Japan ; Department of Japanese Oriental Medicine, Graduate School of Medical and Pharmaceutical Sciences, University of Toyama, Toyama 930-0194, Japan.

ABSTRACT
Obesity has been recognized as one of the most important risk factors for a variety of chronic diseases, such as diabetes, hypertension/cardiovascular diseases, steatosis/hepatitis, and cancer. Keishibukuryogan (KBG, Gui Zhi Fu Ling Wan in Chinese) is a traditional Chinese/Japanese (Kampo) medicine that has been known to improve blood circulation and is also known for its anti-inflammatory or scavenging effect. In this study, we evaluated the effect of KBG in two distinct rodent models of obesity driven by either a genetic (SHR/NDmcr-cp rat model) or dietary (high-fat diet-induced mouse obesity model) mechanism. Although there was no significant effect on the body composition in either the SHR rat or the DIO mouse models, KBG treatment significantly decreased the serum level of leptin and liver TG level in the DIO mouse, but not in the SHR rat model. Furthermore, a lower fat deposition in liver and a smaller size of adipocytes in white adipose tissue were observed in the DIO mice treated with KBG. Importantly, we further found downregulation of genes involved in lipid metabolism in the KBG-treated liver, along with decreased liver TG and cholesterol level. Our present data experimentally support in fact that KBG can be an attractive Kampo medicine to improve obese status through a regulation of systemic leptin level and/or lipid metabolism.

No MeSH data available.


Related in: MedlinePlus

Effect of KBG on serum levels of leptin and insulin in obesity models. (a, b) SHR rats were administered with control water or KBG (500 mg/kg, p.o., daily) for 8 weeks. Serum samples were collected upon the termination and levels of leptin (left) or insulin (right) were measured. (b, c) C57BL/6 mice were fed with normal diet (ND) or high-fat diet (HFD) for 10 weeks and then administered with control water or KBG (500 mg/kg, p.o., daily) for 12 weeks under the same feeding condition. After 8 weeks of control or KBG treatment, mice fed with HFD were changed to ND until the termination of experiment with maintaining KBG treatment for another 4 weeks. Serum samples were collected before the time for food changing (b) or upon the termination (c) and levels of leptin (left) or insulin (right) were measured by using specific ELISA assay. Data are mean ± SEM (n = 7–15). *P < 0.005; **P < 0.001.
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fig3: Effect of KBG on serum levels of leptin and insulin in obesity models. (a, b) SHR rats were administered with control water or KBG (500 mg/kg, p.o., daily) for 8 weeks. Serum samples were collected upon the termination and levels of leptin (left) or insulin (right) were measured. (b, c) C57BL/6 mice were fed with normal diet (ND) or high-fat diet (HFD) for 10 weeks and then administered with control water or KBG (500 mg/kg, p.o., daily) for 12 weeks under the same feeding condition. After 8 weeks of control or KBG treatment, mice fed with HFD were changed to ND until the termination of experiment with maintaining KBG treatment for another 4 weeks. Serum samples were collected before the time for food changing (b) or upon the termination (c) and levels of leptin (left) or insulin (right) were measured by using specific ELISA assay. Data are mean ± SEM (n = 7–15). *P < 0.005; **P < 0.001.

Mentions: We then investigated whether KBG treatment affects the obesity-associated serum biomarkers. While KBG treatment did not show any significant effect on the serum levels of leptin in the SHR rat model (Figure 3(a)), DIO mice treated with KBG showed a significantly lower level of serum leptin, both in chronic disease state (Figure 3(b)) and in combination with diet modification (Figure 3(c)). Neither the SHR rats nor the DIO mice treated with KBG showed any significant alteration in their serum insulin level (Figure 3).


Effect of keishibukuryogan on genetic and dietary obesity models.

Gao F, Yokoyama S, Fujimoto M, Tsuneyama K, Saiki I, Shimada Y, Hayakawa Y - Evid Based Complement Alternat Med (2015)

Effect of KBG on serum levels of leptin and insulin in obesity models. (a, b) SHR rats were administered with control water or KBG (500 mg/kg, p.o., daily) for 8 weeks. Serum samples were collected upon the termination and levels of leptin (left) or insulin (right) were measured. (b, c) C57BL/6 mice were fed with normal diet (ND) or high-fat diet (HFD) for 10 weeks and then administered with control water or KBG (500 mg/kg, p.o., daily) for 12 weeks under the same feeding condition. After 8 weeks of control or KBG treatment, mice fed with HFD were changed to ND until the termination of experiment with maintaining KBG treatment for another 4 weeks. Serum samples were collected before the time for food changing (b) or upon the termination (c) and levels of leptin (left) or insulin (right) were measured by using specific ELISA assay. Data are mean ± SEM (n = 7–15). *P < 0.005; **P < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4352422&req=5

fig3: Effect of KBG on serum levels of leptin and insulin in obesity models. (a, b) SHR rats were administered with control water or KBG (500 mg/kg, p.o., daily) for 8 weeks. Serum samples were collected upon the termination and levels of leptin (left) or insulin (right) were measured. (b, c) C57BL/6 mice were fed with normal diet (ND) or high-fat diet (HFD) for 10 weeks and then administered with control water or KBG (500 mg/kg, p.o., daily) for 12 weeks under the same feeding condition. After 8 weeks of control or KBG treatment, mice fed with HFD were changed to ND until the termination of experiment with maintaining KBG treatment for another 4 weeks. Serum samples were collected before the time for food changing (b) or upon the termination (c) and levels of leptin (left) or insulin (right) were measured by using specific ELISA assay. Data are mean ± SEM (n = 7–15). *P < 0.005; **P < 0.001.
Mentions: We then investigated whether KBG treatment affects the obesity-associated serum biomarkers. While KBG treatment did not show any significant effect on the serum levels of leptin in the SHR rat model (Figure 3(a)), DIO mice treated with KBG showed a significantly lower level of serum leptin, both in chronic disease state (Figure 3(b)) and in combination with diet modification (Figure 3(c)). Neither the SHR rats nor the DIO mice treated with KBG showed any significant alteration in their serum insulin level (Figure 3).

Bottom Line: Obesity has been recognized as one of the most important risk factors for a variety of chronic diseases, such as diabetes, hypertension/cardiovascular diseases, steatosis/hepatitis, and cancer.Keishibukuryogan (KBG, Gui Zhi Fu Ling Wan in Chinese) is a traditional Chinese/Japanese (Kampo) medicine that has been known to improve blood circulation and is also known for its anti-inflammatory or scavenging effect.Importantly, we further found downregulation of genes involved in lipid metabolism in the KBG-treated liver, along with decreased liver TG and cholesterol level.

View Article: PubMed Central - PubMed

Affiliation: Division of Pathogenic Biochemistry, Institute of Natural Medicine, University of Toyama, Toyama 930-0194, Japan ; Department of Japanese Oriental Medicine, Graduate School of Medical and Pharmaceutical Sciences, University of Toyama, Toyama 930-0194, Japan.

ABSTRACT
Obesity has been recognized as one of the most important risk factors for a variety of chronic diseases, such as diabetes, hypertension/cardiovascular diseases, steatosis/hepatitis, and cancer. Keishibukuryogan (KBG, Gui Zhi Fu Ling Wan in Chinese) is a traditional Chinese/Japanese (Kampo) medicine that has been known to improve blood circulation and is also known for its anti-inflammatory or scavenging effect. In this study, we evaluated the effect of KBG in two distinct rodent models of obesity driven by either a genetic (SHR/NDmcr-cp rat model) or dietary (high-fat diet-induced mouse obesity model) mechanism. Although there was no significant effect on the body composition in either the SHR rat or the DIO mouse models, KBG treatment significantly decreased the serum level of leptin and liver TG level in the DIO mouse, but not in the SHR rat model. Furthermore, a lower fat deposition in liver and a smaller size of adipocytes in white adipose tissue were observed in the DIO mice treated with KBG. Importantly, we further found downregulation of genes involved in lipid metabolism in the KBG-treated liver, along with decreased liver TG and cholesterol level. Our present data experimentally support in fact that KBG can be an attractive Kampo medicine to improve obese status through a regulation of systemic leptin level and/or lipid metabolism.

No MeSH data available.


Related in: MedlinePlus