고지방식이 비만마우스에서 越婢加朮湯이 식이효율과 내장지방에 미치는 영향 (WBCEx1 Reduces Feeding Efficiency Ratio and Visceral Obesity in Obese Mice Induced by High Fat Diet)

서지정보

· 발행기관 : 한방재활의학과학회
· 수록지 정보 : 한방재활의학과학회지 / 21권 / 1호 / 1 ~ 22페이지
· 저자명 : 안정란, 강연경, 장동호, 이인선, 신순식, 정혜경, 이희영, 이혜림

초록

Objectives :This study was undertaken to verify the effects of Wolbigachul-tang1(WBCEx1) on obesity using high fat diet-induced male mice and to investigate the molecular mechanisms involved.
Methods :8-week old C57BL/6 mice were divided into 5 groups; lean control, obese control, WBCEx1, 2, 3. After mice were treated with WBCEx1(water extract), 2(30% ethanol extract), 3(water extract; Ephedra sinica Stapf., Gypsum fibrosum) for 12 weeks, body weight gain, feeding efficiency ratio, plasma lipid and glucose metabolism, the messenger RNA(mRNA) expression of peroxisome proliferator activated receptor(PPAR)α target genes were measured. In addition, PPARα target gene expression was examined in liver, white adipose tissue and skeletal muscle.
Results :1. WBCEx1-treated mice had significantly lower body weight gain and feeding efficiency ratio.
2. Consistent with the effects on body weight gain, WBCEx1 decreased the weights of epididymal and retroperitoneal white adipose tissue, inguinal subcutaneous adipose tissue, and brown adipose tissue.
3. WBCEx1 significantly decreased plasma triglyceride and total cholesterol levels.
4. The size of adipocytes were significantly decreased by WBCEx1, whereas the adipocyte number per unit area was increased. Hepatic lipid accumulation was decreased by WBCEx1.
5. WBCEx1 did not affect the mRNA expression of PPARα target genes in liver, adipose tissue, and skeletal muscle.
6. Plasma asparate aminotransferase(AST), alanine aminotransferase(ALT), blood urea nitrogen(BUN) and creatine concentrations were in the physiological range. Liver and kidney weights were significantly lower following WBCEx treatment compared with obese controls, indicating that WBCEx does not show any toxic effects on liver and kidney.
Conclusions :These results suggest that WBCEx1-induced body weight reduction is associated with appetite control and mediated by a mechanism other than the activation of PPARα.

영어초록

Objectives :This study was undertaken to verify the effects of Wolbigachul-tang1(WBCEx1) on obesity using high fat diet-induced male mice and to investigate the molecular mechanisms involved.
Methods :8-week old C57BL/6 mice were divided into 5 groups; lean control, obese control, WBCEx1, 2, 3. After mice were treated with WBCEx1(water extract), 2(30% ethanol extract), 3(water extract; Ephedra sinica Stapf., Gypsum fibrosum) for 12 weeks, body weight gain, feeding efficiency ratio, plasma lipid and glucose metabolism, the messenger RNA(mRNA) expression of peroxisome proliferator activated receptor(PPAR)α target genes were measured. In addition, PPARα target gene expression was examined in liver, white adipose tissue and skeletal muscle.
Results :1. WBCEx1-treated mice had significantly lower body weight gain and feeding efficiency ratio.
2. Consistent with the effects on body weight gain, WBCEx1 decreased the weights of epididymal and retroperitoneal white adipose tissue, inguinal subcutaneous adipose tissue, and brown adipose tissue.
3. WBCEx1 significantly decreased plasma triglyceride and total cholesterol levels.
4. The size of adipocytes were significantly decreased by WBCEx1, whereas the adipocyte number per unit area was increased. Hepatic lipid accumulation was decreased by WBCEx1.
5. WBCEx1 did not affect the mRNA expression of PPARα target genes in liver, adipose tissue, and skeletal muscle.
6. Plasma asparate aminotransferase(AST), alanine aminotransferase(ALT), blood urea nitrogen(BUN) and creatine concentrations were in the physiological range. Liver and kidney weights were significantly lower following WBCEx treatment compared with obese controls, indicating that WBCEx does not show any toxic effects on liver and kidney.
Conclusions :These results suggest that WBCEx1-induced body weight reduction is associated with appetite control and mediated by a mechanism other than the activation of PPARα.

참고자료

· 없음