• 대한한의학방제학회지
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• 제19권2호
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• pp.47-59
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• 2011

Objectives : We investigated the effects of gambigyeongsinhwan2(GGH(2)) on body weight and examined whether blood triglyceride levels and visceral fat are inhibited by it in high fat diet-fed obese male mice. Methods : 8 weeks old, high fat diet-fed obese male mice were divided into 5 groups: C57BL/6N normal, control, GGH(2)-1, GGH(2)-2 and GGH(2)-3. After mice were treated with GGH(2) for 8 weeks, we measured body weight gain, food intake, feeding efficiency ratio, fat weight, plasma leptin and lipid levels. We also did histological analysis for liver and fat on the mice. Results : 1. Compared with controls, GGH(2)-treated mice had lower body weight gain and adipose tissue weight, the magnitudes of which were prominent in GGH(2)-3. 2. Compared with controls, GGH(2)-treated mice had lower feeding efficiency ratio, the magnitude of which was prominent in GGH(2)-3. 3. Compared with controls, GGH(2)-treated mice had lower blood plasma triglyceride level. 4. Blood plasma AST and ALT concentrations were not changed by GGH(2), indicating GGH(2) do not show any toxic effects. 5. Consistent with their effects on body weight gain, the size of adipocytes were significantly decreased by GGH(2), whereas the adipocyte number per unit area was significantly increased, suggesting that GGH(2) decreased the number of large adipocytes. Hepatic lipid accumulation was decreased by GGH(2). Conclusions : These results demonstrate that GGH(2) effectively reduces body weight gain, feeding efficiency ratio, blood plasma triglyceride level and improves abdominal fat.

• 동의생리병리학회지
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• 제27권1호
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• pp.99-106
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• 2013

We investigated the effects of gambigyeongsinhwan(GGH)(4) on body weight and non-alcoholic fatty liver disease(NAFLD) examined whether blood total cholesterol, LDL-cholesterol, free fatty acid and triglyceride levels and hepatic lipid accumulation are inhibited by it in high fat diet-fed obese male mice. 8 weeks old, high fat diet-fed obese male mice were divided into 5 groups: C57BL/6N normal, control, GGH(4)-1, GGH(4)-2 and GGH(4)-3. After mice were treated with GGH(4) for 8 weeks, we measured body weight gain, food intake, feeding efficiency ratio, fat weight, plasma ALT, leptin and lipid levels. We also did histological analysis for liver and fat on the mice. Compared with controls, GGH(4)-treated mice had lower body weight gain and adipose tissue weight, the magnitudes of which were prominent in GGH(4)-2. Compared with controls, GGH(4)-treated mice had lower feeding efficiency ratio and blood leptin level, the magnitudes of which was prominent in GGH(4)-2. Compared with controls, GGH(4)-treated mice had lower blood plasma total cholesterol, LDL-cholesterol, free fatty acid and triglyceride levels. Compared with controls, GGH(4)-2 treated mice had lower blood plasma ALT concentration. Consistent with their effects on body weight gain, the size of adipocytes were significantly decreased by GGH(4), whereas the adipocyte number per unit area was significantly increased, suggesting that GGH(4) decreased the number of large adipocytes. Hepatic lipid accumulation was decreased by GGH(4). In conclusion, these results suggest that GGH(4) exhibits anti-obesity effects through the modulation of feeding efficiency ratio and plasma obesity parameters. Moreover, it seems that GGH(4) also contributes to improve NAFLD through the regulation of plasma ALT and hepatic triglyceride accumulation.

• 대한본초학회지
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• 제29권1호
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• pp.35-43
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• 2014

Objectives : We investigated the effects of gambigyeongsinhwan(GGH)(1) on body weight and non-alcoholic fatty liver disease(NAFLD) examined whether blood total cholesterol, LDL-cholesterol, free fatty acid and triglyceride levels and hepatic lipid accumulation are inhibited by it in high fat diet-fed obese male mice. Methods : 8 weeks old, high fat diet-fed obese male mice were divided into 5 groups: C57BL/6N normal, control, GGH(1)-1, GGH(1)-2 and GGH(1)-3. After mice were treated with GGH(1) for 8 weeks, we measured body weight gain, food intake, feeding efficiency ratio, fat weight, plasma ALT, leptin and lipid levels. We also did histological analysis for liver and fat on the mice. Results : Compared with controls, GGH(1)-treated mice had lower body weight gain and adipose tissue weight, the magnitudes of which were prominent in GGH(1)-3. Compared with controls, GGH(1)-treated mice had lower feeding efficiency ratio and blood leptin level, the magnitudes of which was prominent in GGH(1)-3. Compared with controls, GGH(1)-treated mice had lower blood plasma total cholesterol, LDL-cholesterol, free fatty acid and triglyceride levels. Compared with controls, GGH(1)-3 treated mice had lower blood plasma ALT concentration. Consistent with their effects on body weight gain, the size of adipocytes were significantly decreased by GGH(1), whereas the adipocyte number per unit area was significantly increased, suggesting that GGH(1) decreased the number of large adipocytes. Hepatic lipid accumulation was decreased by GGH(1). Conclusions : In conclusion, these results suggest that GGH(1) exhibits anti-obesity effects through the modulation of feeding efficiency ratio and plasma obesity parameters. Moreover, it seems that GGH(1) also contributes to improve NAFLD through the regulation of plasma ALT and hepatic triglyceride accumulation.

• 대한본초학회지
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• 제28권2호
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• pp.39-44
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• 2013

Objectives : Gambigyeongsinhwan 16 (GGEx16), gambigyeongsinhwan 18 (GGEx18) and gambitongseong capsule are shown to be involved in the regulation of obesity. Therefore, the aim of this study was to compare the reporter activity of anti-obesity genes such as peroxisome proliferator-activated receptor ${\alpha}$ ($PPAR{\alpha}$) and $PPAR{\delta}$ by GGEx16, GGEx18 and gambitongseong capsule. Methods : After NMu2Li liver cells, C2C12 skeletal muscle cells and 3T3-L1 preadipocytes were treated with GGEx16 (1 ${\mu}g/ml$), GGEx18 (1 ${\mu}g/ml$) and different concentrations of gambitongseong capsule, the transactivation of $PPAR{\alpha}$ and $PPAR{\delta}$ was measured by a luciferase reporter gene assay. Results : $PPAR{\alpha}$ reporter gene activity in NMu2Li liver cells and 3T3-L1 preadipocytes was significantly increased by GGEx16, GGEx18 and gambitongseong capsule compared with control, whereas $PPAR{\alpha}$ reporter gene activity in C2C12 skeletal muscle cells was significantly increased by GGEx18 only compared with control. Similarly, $PPAR{\delta}$ reporter gene activity in 3T3-L1 preadipocytes was also significantly increased by GGEx18 compared with control. $PPAR{\delta}$ reporter gene activity in C2C12 skeletal muscle cells was significantly increased by GGEx16 and GGEx18 compared with control although $PPAR{\delta}$ reporter gene activity in NMu2Li liver cells was not changed by these three formulas. Conclusions : These results suggest that all three formulas have the ability to stimulate $PPAR{\alpha}$ and $PPAR{\delta}$ transactivation in animal cell lines with high metabolic rates. In particular, this effects were most prominent in GGEx18-treated cells. In addition, it is likely that GGEx18 may be used as an effective anti-obesity composition.