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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

Histopathological evaluation of fat and liver tissue in DIO mice. 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. (a) Representative images (×200) of H&E staining of liver (upper panels) and white adipose tissue (lower panels) of DIO mice are shown. (b) Steatosis scores of DIO mice. N.D.: not detected. (c) Observed number of adipocyte counts of WAT in DIO mice. Data are mean ± SEM (n = 7–15). **P < 0.001.
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fig5: Histopathological evaluation of fat and liver tissue in DIO mice. 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. (a) Representative images (×200) of H&E staining of liver (upper panels) and white adipose tissue (lower panels) of DIO mice are shown. (b) Steatosis scores of DIO mice. N.D.: not detected. (c) Observed number of adipocyte counts of WAT in DIO mice. Data are mean ± SEM (n = 7–15). **P < 0.001.

Mentions: To further explore the therapeutic benefit of KBG in obesity, we examined the effect of KBG on the expression of liver lipids in both SHR rats and DIO mice. While KBG did not show any significant effect on liver content of TG, cholesterol, and FFA in the SHR rat (Figure 4(a)), the liver TG and cholesterol level (but not FFA level) of the KBG-treated DIO mice were significantly lower than those of the control group (Figure 4(b)). In concert with such a reduction in the liver lipid contents, we observed less adipocyte accumulation in the liver of DIO mice treated with KBG (Figure 5(a), upper panels) and indeed the steatosis score was significantly lower in DIO mice treated with KBG (Figure 5(b)). Furthermore, the size of adipocytes in white adipose tissue, which was enlarged in DIO mice, was relatively smaller with KBG treatment (Figure 5(a), lower panels) as seen in the increased number of adipocytes on histological examination (Figure 5(c)). We then examined the effect of KBG on the mRNA expression of molecules associated with lipid metabolism in liver to understand the potential molecular mechanism that underlies the control of lipid metabolism in KBG-treated DIO mice, by using quantitative real-time PCR. As shown in Figure 6, we found that the mRNA expressions of PPARγ and SREBP1 in the liver were significantly decreased by KBG treatment in DIO mice.


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)

Histopathological evaluation of fat and liver tissue in DIO mice. 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. (a) Representative images (×200) of H&E staining of liver (upper panels) and white adipose tissue (lower panels) of DIO mice are shown. (b) Steatosis scores of DIO mice. N.D.: not detected. (c) Observed number of adipocyte counts of WAT in DIO mice. Data are mean ± SEM (n = 7–15). **P < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4352422&req=5

fig5: Histopathological evaluation of fat and liver tissue in DIO mice. 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. (a) Representative images (×200) of H&E staining of liver (upper panels) and white adipose tissue (lower panels) of DIO mice are shown. (b) Steatosis scores of DIO mice. N.D.: not detected. (c) Observed number of adipocyte counts of WAT in DIO mice. Data are mean ± SEM (n = 7–15). **P < 0.001.
Mentions: To further explore the therapeutic benefit of KBG in obesity, we examined the effect of KBG on the expression of liver lipids in both SHR rats and DIO mice. While KBG did not show any significant effect on liver content of TG, cholesterol, and FFA in the SHR rat (Figure 4(a)), the liver TG and cholesterol level (but not FFA level) of the KBG-treated DIO mice were significantly lower than those of the control group (Figure 4(b)). In concert with such a reduction in the liver lipid contents, we observed less adipocyte accumulation in the liver of DIO mice treated with KBG (Figure 5(a), upper panels) and indeed the steatosis score was significantly lower in DIO mice treated with KBG (Figure 5(b)). Furthermore, the size of adipocytes in white adipose tissue, which was enlarged in DIO mice, was relatively smaller with KBG treatment (Figure 5(a), lower panels) as seen in the increased number of adipocytes on histological examination (Figure 5(c)). We then examined the effect of KBG on the mRNA expression of molecules associated with lipid metabolism in liver to understand the potential molecular mechanism that underlies the control of lipid metabolism in KBG-treated DIO mice, by using quantitative real-time PCR. As shown in Figure 6, we found that the mRNA expressions of PPARγ and SREBP1 in the liver were significantly decreased by KBG treatment in DIO mice.

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