Key result
Ginsenoside-Rb2 treatment in rats transiently decreased hepatic glycogen and increased glucose-6-phosphate and phosphofructokinase activity, alongside lipid accumulation in adipose tissue.
Hypothesis-generating for ginsenoside-Rb2 metabolic effects in rats; human trials needed before clinical relevance.
In order to clarify the mechanism of action of ginsenoside-Rb2 in rats, time course experiments were carried out. The maximum decrease in the hepatic glycogen content was found 8h after the treatment, but the content had nearly recovered to the control level 24h after the treatment. In contrast, the level of hepatic glucose-6-phosphate increased, reaching the maximum at 8h. There was also a dramatic increase in the phosphofructokinase activity, peaking at 12h. In addition, accumulation of lipid in adipose tissue was observed 10-12h after the administration of ginsenoside-Rb2, whereas no significant changes in the total lipid, triglyceride, total cholesterol, phospholipid, glucose, pyruvate, and lactate levels of the liver were observed throughout the experimental period. An increase of hepatic glucose-6-phosphate dehydrogenase activity was observed 2-4h after the treatment, but this response was transitory.
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Yokozawa et al. (1984) studied this question. ginsenoside-Rb2 vs. control was evaluated on hepatic glycogen content, glucose-6-phosphate, phosphofructokinase activity, and lipid accumulation. Ginsenoside-Rb2 treatment in rats transiently decreased hepatic glycogen and increased glucose-6-phosphate and phosphofructokinase activity, alongside lipid accumulation in adipose tissue.
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