AIMS: We observed whether the anti-obesity activity of yeast hydrolysate (YH) was due to the alteration of lipid-regulating enzyme activities. METHODS: Male ICR mice were divided into four groups: a normal diet group (ND; 4.2% fat), a high-fat diet group (HF; 27.7% fat), an HF group treated orally with 0.5% or 1% YH in the drinking water (HF+YH0.5; 27.7% fat and HF+YH1; 27.7% fat). RESULTS: After 5 weeks, the YH groups (HF+YH0.5=3.92±0.17 g/100 g BW and HF+YH1=3.76±0.13 g/100 g BW) had significantly lower levels of epididymal fats compared to the HF group (4.91±0.29 g/100 g BW; p<0.05). YH supplementation produced a decrease in serum triglycerides and low-density lipoprotein cholesterol concentrations and body weight gain, and produced a dose-dependent significant increase in serum ghrelin compared with the HF group (p<0.05). Hepatic glucose-6-phosphate dehydrogenase (G6PD) activity was inhibited by YH supplementation compared with the HF group, and mice treated orally with 1% YH exhibited a significant decrease in hepatic malic enzyme (ME) activity compared to obese mice treated with the vehicle (HF=10.44±2.74 nmol/min/mg protein vs. HF+YH1=6.68±2.23 nmol/min/mg protein; p<0.05). CONCLUSIONS: YH supplementation suppressed body fat accumulation by attenuating fatty acid synthesis through the downregulation of hepatic G6PD and ME activities.
AIMS: We observed whether the anti-obesity activity of yeast hydrolysate (YH) was due to the alteration of lipid-regulating enzyme activities. METHODS: Male ICR mice were divided into four groups: a normal diet group (ND; 4.2% fat), a high-fat diet group (HF; 27.7% fat), an HF group treated orally with 0.5% or 1% YH in the drinking water (HF+YH0.5; 27.7% fat and HF+YH1; 27.7% fat). RESULTS: After 5 weeks, the YH groups (HF+YH0.5=3.92±0.17 g/100 g BW and HF+YH1=3.76±0.13 g/100 g BW) had significantly lower levels of epididymal fats compared to the HF group (4.91±0.29 g/100 g BW; p<0.05). YH supplementation produced a decrease in serum triglycerides and low-density lipoprotein cholesterol concentrations and body weight gain, and produced a dose-dependent significant increase in serum ghrelin compared with the HF group (p<0.05). Hepatic glucose-6-phosphate dehydrogenase (G6PD) activity was inhibited by YH supplementation compared with the HF group, and mice treated orally with 1% YH exhibited a significant decrease in hepatic malic enzyme (ME) activity compared to obesemice treated with the vehicle (HF=10.44±2.74 nmol/min/mg protein vs. HF+YH1=6.68±2.23 nmol/min/mg protein; p<0.05). CONCLUSIONS:YH supplementation suppressed body fat accumulation by attenuating fatty acid synthesis through the downregulation of hepatic G6PD and ME activities.