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Kaempferia parviflora extract increases energy consumption through activation of BAT in mice.

Yoshino S, Kim M, Awa R, Kuwahara H, Kano Y, Kawada T - Food Sci Nutr (2014)

Bottom Line: For both 0.5% KPE and 1.0% KPE, 7 weeks' feeding of KPE contained in a high-fat diet (HFD) significantly decreased body weight gain, intraabdominal fat accumulation, and plasma triglyceride and leptin levels.We also found that 1.0% KPE feeding significantly increased the uncoupling protein 1 (UCP1) expression in brown adipose tissue (BAT).These results demonstrate that KPE promotes energy metabolism by activation of BAT, at both doses and up-regulation of UCP1 protein at a high dose.

View Article: PubMed Central - PubMed

Affiliation: Research Center, Maruzen Pharmaceuticals Co., Ltd. Fukuyama, Hiroshima, 729-3102, Japan.

ABSTRACT
Kaempferia parviflora (KP) is a member of the ginger family and is known in Thailand as Thai ginseng, Krachai Dam or Black Ginger. TheK. parviflora extract (KPE) was previously reported to have a number of physiological effects; however, the antiobesity effects of KPE and its mechanisms remain to be elucidated. In this study, we conducted KPE feeding experiments (low dose: 0.5% KPE, high dose: 1.0% KPE) in mice to examine the antiobesity effects. For both 0.5% KPE and 1.0% KPE, 7 weeks' feeding of KPE contained in a high-fat diet (HFD) significantly decreased body weight gain, intraabdominal fat accumulation, and plasma triglyceride and leptin levels. Concurrently, KPE administration increased oxygen consumption in mice fed on a HFD. We also found that 1.0% KPE feeding significantly increased the uncoupling protein 1 (UCP1) expression in brown adipose tissue (BAT). Moreover, KPE administration increased urinary noradrenaline secretion levels. These results demonstrate that KPE promotes energy metabolism by activation of BAT, at both doses and up-regulation of UCP1 protein at a high dose. Although numerous challenges remain, the present study demonstrated that KPE suppresses HFD-induced obesity through increased energy metabolism.

No MeSH data available.


Related in: MedlinePlus

KPE increases urinary noradrenaline secretion in C57BL/6J mice. Urinary noradrenaline (A) and adrenaline (B) secretion in C57BL/6J mice with 0.5% KPE treatment (n = 8) and without KPE treatment (n = 6) for 2 weeks under HFD feeding. Urinary adrenaline and noradrenaline levels were measured by HPLC analysis. These procedures were aproved by the Institutional Animal Care and Use Committee of Kobe Women's University, Faculty of Home Economics (A316). Each bar represents means ± SE *P < 0.05 compared with untreated control group. KPE,K. parviflora extract.
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fig03: KPE increases urinary noradrenaline secretion in C57BL/6J mice. Urinary noradrenaline (A) and adrenaline (B) secretion in C57BL/6J mice with 0.5% KPE treatment (n = 8) and without KPE treatment (n = 6) for 2 weeks under HFD feeding. Urinary adrenaline and noradrenaline levels were measured by HPLC analysis. These procedures were aproved by the Institutional Animal Care and Use Committee of Kobe Women's University, Faculty of Home Economics (A316). Each bar represents means ± SE *P < 0.05 compared with untreated control group. KPE,K. parviflora extract.

Mentions: UCP1 expression is regulated by sympathetic nerve activity (Mory et al. 1984; Feldmann et al. 2009). We hypothesized that KPE activates the sympathetic nerves. To test this hypothesis, we measured urinary concentrations of adrenaline and noradrenaline using the previously used method (Davidson and Fitzpartrick 1985), which are secreted upon sympathetic nerve activation. In this study, 2 weeks administration of 0.5% KPE significantly increased urinary noradrenaline secretion in C57BL/6J mice (Fig.3A). The results of the present experiment suggest that KPE feeding promoted noradrenaline secretion, thereby increasing triglyceride decomposition and leading to a decrease in serum triglyceride levels. It is known that adrenaline and noradrenaline cause an increase in cyclic adenosine monophosphate (cAMP) levels in adipocytes, and that cAMP regulates UCP1 expression via PKA (Cannon and Lindberg 1979). These results suggest that KPE consumption has antiobesity effects.


Kaempferia parviflora extract increases energy consumption through activation of BAT in mice.

Yoshino S, Kim M, Awa R, Kuwahara H, Kano Y, Kawada T - Food Sci Nutr (2014)

KPE increases urinary noradrenaline secretion in C57BL/6J mice. Urinary noradrenaline (A) and adrenaline (B) secretion in C57BL/6J mice with 0.5% KPE treatment (n = 8) and without KPE treatment (n = 6) for 2 weeks under HFD feeding. Urinary adrenaline and noradrenaline levels were measured by HPLC analysis. These procedures were aproved by the Institutional Animal Care and Use Committee of Kobe Women's University, Faculty of Home Economics (A316). Each bar represents means ± SE *P < 0.05 compared with untreated control group. KPE,K. parviflora extract.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4256566&req=5

fig03: KPE increases urinary noradrenaline secretion in C57BL/6J mice. Urinary noradrenaline (A) and adrenaline (B) secretion in C57BL/6J mice with 0.5% KPE treatment (n = 8) and without KPE treatment (n = 6) for 2 weeks under HFD feeding. Urinary adrenaline and noradrenaline levels were measured by HPLC analysis. These procedures were aproved by the Institutional Animal Care and Use Committee of Kobe Women's University, Faculty of Home Economics (A316). Each bar represents means ± SE *P < 0.05 compared with untreated control group. KPE,K. parviflora extract.
Mentions: UCP1 expression is regulated by sympathetic nerve activity (Mory et al. 1984; Feldmann et al. 2009). We hypothesized that KPE activates the sympathetic nerves. To test this hypothesis, we measured urinary concentrations of adrenaline and noradrenaline using the previously used method (Davidson and Fitzpartrick 1985), which are secreted upon sympathetic nerve activation. In this study, 2 weeks administration of 0.5% KPE significantly increased urinary noradrenaline secretion in C57BL/6J mice (Fig.3A). The results of the present experiment suggest that KPE feeding promoted noradrenaline secretion, thereby increasing triglyceride decomposition and leading to a decrease in serum triglyceride levels. It is known that adrenaline and noradrenaline cause an increase in cyclic adenosine monophosphate (cAMP) levels in adipocytes, and that cAMP regulates UCP1 expression via PKA (Cannon and Lindberg 1979). These results suggest that KPE consumption has antiobesity effects.

Bottom Line: For both 0.5% KPE and 1.0% KPE, 7 weeks' feeding of KPE contained in a high-fat diet (HFD) significantly decreased body weight gain, intraabdominal fat accumulation, and plasma triglyceride and leptin levels.We also found that 1.0% KPE feeding significantly increased the uncoupling protein 1 (UCP1) expression in brown adipose tissue (BAT).These results demonstrate that KPE promotes energy metabolism by activation of BAT, at both doses and up-regulation of UCP1 protein at a high dose.

View Article: PubMed Central - PubMed

Affiliation: Research Center, Maruzen Pharmaceuticals Co., Ltd. Fukuyama, Hiroshima, 729-3102, Japan.

ABSTRACT
Kaempferia parviflora (KP) is a member of the ginger family and is known in Thailand as Thai ginseng, Krachai Dam or Black Ginger. TheK. parviflora extract (KPE) was previously reported to have a number of physiological effects; however, the antiobesity effects of KPE and its mechanisms remain to be elucidated. In this study, we conducted KPE feeding experiments (low dose: 0.5% KPE, high dose: 1.0% KPE) in mice to examine the antiobesity effects. For both 0.5% KPE and 1.0% KPE, 7 weeks' feeding of KPE contained in a high-fat diet (HFD) significantly decreased body weight gain, intraabdominal fat accumulation, and plasma triglyceride and leptin levels. Concurrently, KPE administration increased oxygen consumption in mice fed on a HFD. We also found that 1.0% KPE feeding significantly increased the uncoupling protein 1 (UCP1) expression in brown adipose tissue (BAT). Moreover, KPE administration increased urinary noradrenaline secretion levels. These results demonstrate that KPE promotes energy metabolism by activation of BAT, at both doses and up-regulation of UCP1 protein at a high dose. Although numerous challenges remain, the present study demonstrated that KPE suppresses HFD-induced obesity through increased energy metabolism.

No MeSH data available.


Related in: MedlinePlus