Tags

Type your tag names separated by a space and hit enter

Ginsenoside Re reduces insulin resistance through inhibition of c-Jun NH2-terminal kinase and nuclear factor-kappaB.
Mol Endocrinol. 2008 Jan; 22(1):186-95.ME

Abstract

Ginsenoside Re (Re), a compound derived from Panax ginseng, shows an antidiabetic effect. However, the molecular basis of its action remains unknown. We investigated insulin signaling and the antiinflammatory effect by Re in 3T3-L1 adipocytes and in high-fat diet (HFD) rats to dissect its anti-hyperglycemic mechanism. Glucose uptake was measured in 3T3-L1 cells and glucose infusion rate determined by clamp in HFD rats. The insulin signaling cascade, including insulin receptor (IR) beta-subunit, IR substrate-1, phosphatidylinositol 3-kinase, Akt and Akt substrate of 160 kDa, and glucose transporter-4 translocation are examined. Furthermore, c-Jun NH(2)-terminal kinase (JNK), MAPK, and nuclear factor (NF)-kappaB signaling cascades were also assessed. The results show Re increases glucose uptake in 3T3-L1 cells and glucose infusion rate in HFD rats. The activation of insulin signaling by Re is initiated at IR substrate-1 and further passes on through phosphatidylinositol 3-kinase and downstream signaling cascades. Moreover, Re demonstrates an impressive suppression of JNK and NF-kappaB activation and inhibitor of NF-kappaBalpha degradation. In conclusion, Re reduces insulin resistance in 3T3-L1 adipocytes and HFD rats through inhibition of JNK and NF-kappaB activation.

Authors+Show Affiliations

Laboratory of Endocrinology and Metabolism, Institute of Health Sciences, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, 197 Rui-Jin 2nd Road, Shanghai 200025, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

17885204

Citation

Zhang, Zhiguo, et al. "Ginsenoside Re Reduces Insulin Resistance Through Inhibition of c-Jun NH2-terminal Kinase and Nuclear Factor-kappaB." Molecular Endocrinology (Baltimore, Md.), vol. 22, no. 1, 2008, pp. 186-95.
Zhang Z, Li X, Lv W, et al. Ginsenoside Re reduces insulin resistance through inhibition of c-Jun NH2-terminal kinase and nuclear factor-kappaB. Mol Endocrinol. 2008;22(1):186-95.
Zhang, Z., Li, X., Lv, W., Yang, Y., Gao, H., Yang, J., Shen, Y., & Ning, G. (2008). Ginsenoside Re reduces insulin resistance through inhibition of c-Jun NH2-terminal kinase and nuclear factor-kappaB. Molecular Endocrinology (Baltimore, Md.), 22(1), 186-95.
Zhang Z, et al. Ginsenoside Re Reduces Insulin Resistance Through Inhibition of c-Jun NH2-terminal Kinase and Nuclear Factor-kappaB. Mol Endocrinol. 2008;22(1):186-95. PubMed PMID: 17885204.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ginsenoside Re reduces insulin resistance through inhibition of c-Jun NH2-terminal kinase and nuclear factor-kappaB. AU - Zhang,Zhiguo, AU - Li,Xiaoying, AU - Lv,Wenshan, AU - Yang,Yisheng, AU - Gao,Hong, AU - Yang,Jun, AU - Shen,Yun, AU - Ning,Guang, Y1 - 2007/09/20/ PY - 2007/9/22/pubmed PY - 2008/7/1/medline PY - 2007/9/22/entrez SP - 186 EP - 95 JF - Molecular endocrinology (Baltimore, Md.) JO - Mol. Endocrinol. VL - 22 IS - 1 N2 - Ginsenoside Re (Re), a compound derived from Panax ginseng, shows an antidiabetic effect. However, the molecular basis of its action remains unknown. We investigated insulin signaling and the antiinflammatory effect by Re in 3T3-L1 adipocytes and in high-fat diet (HFD) rats to dissect its anti-hyperglycemic mechanism. Glucose uptake was measured in 3T3-L1 cells and glucose infusion rate determined by clamp in HFD rats. The insulin signaling cascade, including insulin receptor (IR) beta-subunit, IR substrate-1, phosphatidylinositol 3-kinase, Akt and Akt substrate of 160 kDa, and glucose transporter-4 translocation are examined. Furthermore, c-Jun NH(2)-terminal kinase (JNK), MAPK, and nuclear factor (NF)-kappaB signaling cascades were also assessed. The results show Re increases glucose uptake in 3T3-L1 cells and glucose infusion rate in HFD rats. The activation of insulin signaling by Re is initiated at IR substrate-1 and further passes on through phosphatidylinositol 3-kinase and downstream signaling cascades. Moreover, Re demonstrates an impressive suppression of JNK and NF-kappaB activation and inhibitor of NF-kappaBalpha degradation. In conclusion, Re reduces insulin resistance in 3T3-L1 adipocytes and HFD rats through inhibition of JNK and NF-kappaB activation. SN - 0888-8809 UR - https://www.unboundmedicine.com/medline/citation/17885204/Ginsenoside_Re_reduces_insulin_resistance_through_inhibition_of_c_Jun_NH2_terminal_kinase_and_nuclear_factor_kappaB_ L2 - https://academic.oup.com/mend/article-lookup/doi/10.1210/me.2007-0119 DB - PRIME DP - Unbound Medicine ER -