Original Article

Hypoglycemic mechanism of ginseng glycopeptide.

Ben-Xiang Wang, Qiu-Li Zhou, Ming Yang, Yan Wang, Zhi-Yong Cui, Yong-Qiang Liu, Takashi Ikejima


AIM: To study the hypoglycemic mechanism of ginseng glycopeptide (GGP). METHODS: After administration of GGP, the levels of insulin, lactate dehydrogenase (LDH), lactic acid (LC), and oxygen consumption, as well as blood glucose (BG) and liver glycogen (LG) were measured. Based on these measurement results, the effects of GGP on insulin secretion and anaerobic/aerobic glycolysis were evaluated. Adenylate cyclase (AC) activity and cAMP level were measured to study the effects of GGP on BG and LG metabolism and to determine whether the effects were through second transmitting message system. Propranolol (beta-receptor antagonist) and phentolamine (alpha-receptor antagonist) were used to investigate whether hypoglycemic activity of GGP was through beta- or alpha-adrenoceptor. [3H]DHA (antagonist of beta-adrenoceptor) was used to determine GGP binding affinity to beta-adrenoceptor. Citrate synthetase (CTS), succinate dehydrogenase (SDH), malate dehydrogenase (MDH), and cytochrome oxidase (CCO) activities were measured to explore GGP effects on aerobic glycolysis in liver mitochondria. Phosphorylase (PP) activity was measured to study GGP effects on liver glycogen metabolism. RESULTS: cAMP content and AC activity were increased when BG and LG contents in liver of mice decreased. The decrease in liver glycogen induced by GGP was inhibited by pretreatment with propranolol. Radioligand receptor assay showed that GGP was competing in vitro with [3H]DHA to bind to beta-adrenoceptor of duck erythrocyte membrane, and IC50 of GGP was 63 nmol/L. GGP inhibited LDH activity at an appropriate dosage, at which contents of BG and LG could be effectively lowered. GGP also stimulated activities of SDH, MDH, CCO, CTS, and PP. CONCLUSION: The hypoglycemic activity of GGP may be attributed to the enhancement of aerobic glycolysis through stimulation of beta-adrenoceptor and increase of various rate-limiting enzyme activities related to tricarboxylic acid cycle.

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