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Regulation of signaling molecules associated with insulin action, insulin secretion and pancreatic β-cell mass in the hypoglycemic effects of Korean red ginseng in Goto-Kakizaki rats
- Kim, Hye Young, Kim, Kyong
- Journal of ethnopharmacology 2012 v.142 no.1 pp. 53-58
- Panax, Western blotting, adipose tissue, blood glucose, diabetes mellitus, glucose transporters, glycemic effect, insulin, insulin secretion, muscle tissues, protein synthesis, protein-tyrosine-phosphatase, rats
- ETHNOPHARMACOLOGICAL RELEVANCE: Korean red ginseng (KRG) has long history as herbal remedy for antidiabetic effect. AIM OF THE STUDY: To study molecular mechanisms by which KRG ameliorates diabetes mellitus, we investigated whether the supplementation with the aqueous extract of KRG as a dietary admixture (1%, w/w) regulates the expressions of signaling molecules that are associated with insulin action, insulin secretion and pancreatic β-cell mass in spontaneously diabetic Goto-Kakizaki (GK) rats. METHODS: An aqueous extract of KRG was supplemented for the estimated dosage to be 0.2g/kg rat/day beginning at 5 weeks of age for 12 weeks in male GK rats. Plasma glucose levels were measured every 4 weeks. The expressions of signaling molecules that are associated with insulin action, insulin secretion and β-cell mass in tissues were determined by Western blotting. RESULTS: The 12-week supplementation with KRG significantly (P<0.05) decreased blood glucose compared to control. It up-regulated the expression of glucose transporter (GLUT) 4 in adipose tissue, and down-regulated the expression of protein tyrosine phosphatases (PTP)-1B in adipose tissue and skeletal muscle. It also up-regulated the expression of insulin and down-regulated the expression of uncoupling protein (UCP) 2, Bax and poly (ADP-ribose) polymerase (PARP) in pancreas. CONCLUSIONS: These results suggest that GLUT4, PTP-1B, insulin, UCP2, Bax and PARP may be the primary targets of KRG that result in increase in insulin action and in insulin secretion, and decrease in β-cell mass, and that cause the normalization in glucose homeostasis.