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Effects of compound K on hyperglycemia and insulin resistance in rats with type 2 diabetes mellitus.
Fitoterapia. 2014 Jun; 95:58-64.F

Abstract

Compound K (CK) is a final metabolite of panaxadiol ginsenosides from Panax ginseng. Although anti-diabetic activity of CK has been reported in recent years, the molecular mechanism of CK in the treatment of diabetes mellitus remains unclear. In the present investigation, we established a rat model of type 2 diabetes mellitus (T2DM) with insulin resistance using high-fat diet (HFD) and streptozotocin (STZ), and attempted to verify more details and exact mechanisms in the treatment of T2DM. CK was administered orally at three doses [300, 100 and 30 mg/kg bodyweight (b.w.)] to the diabetic rats. Bodyweight, food-intake, fasting blood glucose (FBG), fasting serum insulin (FINS), insulin sensitivity (ISI), total glycerin (TG), total cholesterol (TC), as well as oral glucose tolerance test (OGTT) were evaluated in normal and diabetic rats. According to our results, CK could improve bodyweight and food-intake of diabetic rats. CK exhibited dose-dependent reduction of FBG, TG and TC of diabetic rats. CK treatment also enhanced FINS and ISI. Meanwhile, the glucose tolerance observed in the present study was improved significantly by CK. It is concluded from the results that CK may have improving effects on hyperglycemia and insulin resistance of diabetic rats. Furthermore, research showed that CK could promote the expression of InsR, IRS1, PI3Kp85, pAkt and Glut4 in skeletal muscle tissue of diabetic rats. These results indicate that the hypoglycemic activity of CK is mediated by improvement of insulin sensitivity, which is closely related to PI3K/Akt signaling pathway.

Authors+Show Affiliations

College of Pharmacy, Beihua University, Jilin, Jilin 132013, PR China; College of Basic Medical Sciences, Changchun University of Chinese Medicine, Changchun, Jilin 130117, PR China. Electronic address: jiangshuang_2000@163.com.College of Food Science and Engineering, Jilin Agricultural University, Changchun, Jilin 130117, PR China.Department of Personnel, Changchun University of Chinese Medicine, Changchun, Jilin 130117, PR China.College of Pharmacy, Beihua University, Jilin, Jilin 132013, PR China; Biological Macromolecular Function Development and Application of Engineering Laboratory, Jilin, Jilin 132013, PR China.College of Pharmacy, Beihua University, Jilin, Jilin 132013, PR China; Biological Macromolecular Function Development and Application of Engineering Laboratory, Jilin, Jilin 132013, PR China.College of Pharmacy, Beihua University, Jilin, Jilin 132013, PR China.College of Pharmacy, Beihua University, Jilin, Jilin 132013, PR China.College of Pharmacy, Beihua University, Jilin, Jilin 132013, PR China.College of Pharmacy, Beihua University, Jilin, Jilin 132013, PR China. Electronic address: alp960@126.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24613802

Citation

Jiang, Shuang, et al. "Effects of Compound K On Hyperglycemia and Insulin Resistance in Rats With Type 2 Diabetes Mellitus." Fitoterapia, vol. 95, 2014, pp. 58-64.
Jiang S, Ren D, Li J, et al. Effects of compound K on hyperglycemia and insulin resistance in rats with type 2 diabetes mellitus. Fitoterapia. 2014;95:58-64.
Jiang, S., Ren, D., Li, J., Yuan, G., Li, H., Xu, G., Han, X., Du, P., & An, L. (2014). Effects of compound K on hyperglycemia and insulin resistance in rats with type 2 diabetes mellitus. Fitoterapia, 95, 58-64. https://doi.org/10.1016/j.fitote.2014.02.017
Jiang S, et al. Effects of Compound K On Hyperglycemia and Insulin Resistance in Rats With Type 2 Diabetes Mellitus. Fitoterapia. 2014;95:58-64. PubMed PMID: 24613802.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of compound K on hyperglycemia and insulin resistance in rats with type 2 diabetes mellitus. AU - Jiang,Shuang, AU - Ren,Dayong, AU - Li,Jianrui, AU - Yuan,Guangxin, AU - Li,Hongyu, AU - Xu,Guangyu, AU - Han,Xiao, AU - Du,Peige, AU - An,Liping, Y1 - 2014/03/05/ PY - 2014/01/10/received PY - 2014/02/24/revised PY - 2014/02/25/accepted PY - 2014/3/12/entrez PY - 2014/3/13/pubmed PY - 2015/1/8/medline KW - Compound K KW - Hyperglycemia KW - Insulin resistance SP - 58 EP - 64 JF - Fitoterapia JO - Fitoterapia VL - 95 N2 - Compound K (CK) is a final metabolite of panaxadiol ginsenosides from Panax ginseng. Although anti-diabetic activity of CK has been reported in recent years, the molecular mechanism of CK in the treatment of diabetes mellitus remains unclear. In the present investigation, we established a rat model of type 2 diabetes mellitus (T2DM) with insulin resistance using high-fat diet (HFD) and streptozotocin (STZ), and attempted to verify more details and exact mechanisms in the treatment of T2DM. CK was administered orally at three doses [300, 100 and 30 mg/kg bodyweight (b.w.)] to the diabetic rats. Bodyweight, food-intake, fasting blood glucose (FBG), fasting serum insulin (FINS), insulin sensitivity (ISI), total glycerin (TG), total cholesterol (TC), as well as oral glucose tolerance test (OGTT) were evaluated in normal and diabetic rats. According to our results, CK could improve bodyweight and food-intake of diabetic rats. CK exhibited dose-dependent reduction of FBG, TG and TC of diabetic rats. CK treatment also enhanced FINS and ISI. Meanwhile, the glucose tolerance observed in the present study was improved significantly by CK. It is concluded from the results that CK may have improving effects on hyperglycemia and insulin resistance of diabetic rats. Furthermore, research showed that CK could promote the expression of InsR, IRS1, PI3Kp85, pAkt and Glut4 in skeletal muscle tissue of diabetic rats. These results indicate that the hypoglycemic activity of CK is mediated by improvement of insulin sensitivity, which is closely related to PI3K/Akt signaling pathway. SN - 1873-6971 UR - https://www.unboundmedicine.com/medline/citation/24613802/Effects_of_compound_K_on_hyperglycemia_and_insulin_resistance_in_rats_with_type_2_diabetes_mellitus_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0367-326X(14)00062-8 DB - PRIME DP - Unbound Medicine ER -