Limits...
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 oxygen consumption and UCP1 expression levels of BAT in C57BL/6J mice. (A) Oxygen consumption of C57BL/6J mice orally administered KPE (0, 0.035 or 0.105 mg/g body weight). Oxygen consumption was measured every 8 min for 24 h using an indirect calorimetric system (Oxymax; Columbus Instruments, Columbus, OH). Each bar represents the mean ± SE (n = 8). *P < 0.05 compared with the untreated control group. (B) UCP1 expression levels of BAT mitochondria in C57BL/6J mice with and without KPE (0.5% and 1.0%) treatment for 7 weeks under HFD feeding. BAT mitochondria were isolated and purified as reported previously, and the total protein content in BAT mitochondria was measured with DC Protein Assay Kit (Bio-Rad, CA). UCP1 expression levels in the mitochondrial fraction were measured by western blotting analysis. A mitochondrial extract from BAT was subjected to SDS-PAGE. UCP1 expression levels in the untreated control group were set at 100%, and relative UCP1 expression levels were presented as the fold induction relative to that of the untreated control group. Each bar represents means ± SE (n = 8). *P < 0.05 compared with untreated control group. UCP1, uncoupling protein 1; BAT, brown adipose tissue; KPE,K. parviflora extract.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4256566&req=5

fig02: KPE increases oxygen consumption and UCP1 expression levels of BAT in C57BL/6J mice. (A) Oxygen consumption of C57BL/6J mice orally administered KPE (0, 0.035 or 0.105 mg/g body weight). Oxygen consumption was measured every 8 min for 24 h using an indirect calorimetric system (Oxymax; Columbus Instruments, Columbus, OH). Each bar represents the mean ± SE (n = 8). *P < 0.05 compared with the untreated control group. (B) UCP1 expression levels of BAT mitochondria in C57BL/6J mice with and without KPE (0.5% and 1.0%) treatment for 7 weeks under HFD feeding. BAT mitochondria were isolated and purified as reported previously, and the total protein content in BAT mitochondria was measured with DC Protein Assay Kit (Bio-Rad, CA). UCP1 expression levels in the mitochondrial fraction were measured by western blotting analysis. A mitochondrial extract from BAT was subjected to SDS-PAGE. UCP1 expression levels in the untreated control group were set at 100%, and relative UCP1 expression levels were presented as the fold induction relative to that of the untreated control group. Each bar represents means ± SE (n = 8). *P < 0.05 compared with untreated control group. UCP1, uncoupling protein 1; BAT, brown adipose tissue; KPE,K. parviflora extract.

Mentions: C57BL6J male mice were fed a high-fat diet (HFD; 60 kcal % fat) containing KPE (0.5 or 1.0%) for 7 weeks. In this study, both 0.5% KPE and 1.0% KPE administration significantly suppressed body weight gain and intraabdominal fat (Fig.1A and B) and decreased serum triglyceride and leptin levels (Table S1). Leptin levels are known to correlate with weight and amount of visceral fat in mice and humans (Shimizu et al. 1997; Ahren 1999); the results from the present study are consistent with these previous reports (Fig.1 and Table S1). In these experiments, there were no differences in total calories consumed during the study period (Fig. S1), suggesting that the reason for the loss of weight and intraabdominal fat was an increase in energy consumption. To explore this possibility, we examined changes in oxygen consumption using the previous method (Goto et al. 2012) after oral administration of KPE (low dose; 0.035 mg/g, high dose; 0.105 mg/g) (Fig.2A). Oxygen consumption after administration was significantly higher in mice treated with KPE. This result indicates that KPE increases oxygen consumption, thus this is one mechanism contributing to its 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 oxygen consumption and UCP1 expression levels of BAT in C57BL/6J mice. (A) Oxygen consumption of C57BL/6J mice orally administered KPE (0, 0.035 or 0.105 mg/g body weight). Oxygen consumption was measured every 8 min for 24 h using an indirect calorimetric system (Oxymax; Columbus Instruments, Columbus, OH). Each bar represents the mean ± SE (n = 8). *P < 0.05 compared with the untreated control group. (B) UCP1 expression levels of BAT mitochondria in C57BL/6J mice with and without KPE (0.5% and 1.0%) treatment for 7 weeks under HFD feeding. BAT mitochondria were isolated and purified as reported previously, and the total protein content in BAT mitochondria was measured with DC Protein Assay Kit (Bio-Rad, CA). UCP1 expression levels in the mitochondrial fraction were measured by western blotting analysis. A mitochondrial extract from BAT was subjected to SDS-PAGE. UCP1 expression levels in the untreated control group were set at 100%, and relative UCP1 expression levels were presented as the fold induction relative to that of the untreated control group. Each bar represents means ± SE (n = 8). *P < 0.05 compared with untreated control group. UCP1, uncoupling protein 1; BAT, brown adipose tissue; KPE,K. parviflora extract.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig02: KPE increases oxygen consumption and UCP1 expression levels of BAT in C57BL/6J mice. (A) Oxygen consumption of C57BL/6J mice orally administered KPE (0, 0.035 or 0.105 mg/g body weight). Oxygen consumption was measured every 8 min for 24 h using an indirect calorimetric system (Oxymax; Columbus Instruments, Columbus, OH). Each bar represents the mean ± SE (n = 8). *P < 0.05 compared with the untreated control group. (B) UCP1 expression levels of BAT mitochondria in C57BL/6J mice with and without KPE (0.5% and 1.0%) treatment for 7 weeks under HFD feeding. BAT mitochondria were isolated and purified as reported previously, and the total protein content in BAT mitochondria was measured with DC Protein Assay Kit (Bio-Rad, CA). UCP1 expression levels in the mitochondrial fraction were measured by western blotting analysis. A mitochondrial extract from BAT was subjected to SDS-PAGE. UCP1 expression levels in the untreated control group were set at 100%, and relative UCP1 expression levels were presented as the fold induction relative to that of the untreated control group. Each bar represents means ± SE (n = 8). *P < 0.05 compared with untreated control group. UCP1, uncoupling protein 1; BAT, brown adipose tissue; KPE,K. parviflora extract.
Mentions: C57BL6J male mice were fed a high-fat diet (HFD; 60 kcal % fat) containing KPE (0.5 or 1.0%) for 7 weeks. In this study, both 0.5% KPE and 1.0% KPE administration significantly suppressed body weight gain and intraabdominal fat (Fig.1A and B) and decreased serum triglyceride and leptin levels (Table S1). Leptin levels are known to correlate with weight and amount of visceral fat in mice and humans (Shimizu et al. 1997; Ahren 1999); the results from the present study are consistent with these previous reports (Fig.1 and Table S1). In these experiments, there were no differences in total calories consumed during the study period (Fig. S1), suggesting that the reason for the loss of weight and intraabdominal fat was an increase in energy consumption. To explore this possibility, we examined changes in oxygen consumption using the previous method (Goto et al. 2012) after oral administration of KPE (low dose; 0.035 mg/g, high dose; 0.105 mg/g) (Fig.2A). Oxygen consumption after administration was significantly higher in mice treated with KPE. This result indicates that KPE increases oxygen consumption, thus this is one mechanism contributing to its 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