Document Detail


The triterpenoid 2-cyano-3,12-dioxooleana-1,9-dien-28-oic-acid methyl ester has potent anti-diabetic effects in diet-induced diabetic mice and Lepr(db/db) mice.
MedLine Citation:
PMID:  20956520     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The triterpenoid 2-Cyano-3,12-dioxooleana-1,9-dien-28-oic-acid (CDDO) and its methyl ester (CDDO-Me) are undergoing clinical trials in cancer and leukemia therapy. Here we report that CDDO-Me ameliorates diabetes in high fat diet-fed type 2 diabetic mice and in Lepr(db/db) mice. CDDO-Me reduces proinflammatory cytokine expression in these animals. Oral CDDO-Me administration reduces total body fat, plasma triglyceride, and free fatty acid levels. It also improves glucose tolerance and insulin tolerance tests. Its potent glucose-lowering activity results from enhanced insulin action. Hyperinsulinemic-euglycemic clamp reveals an increased glucose infusion rate required to maintain euglycemia and showed a significant increase in muscle-specific insulin-stimulated glucose uptake (71% soleus, 58% gastrocnemius) and peripheral glucose clearance as documented by a 48% increase in glucose disposal rate. CDDO-Me activates AMP-activated protein kinase (AMPK) and via LKB1 activation in muscle and liver in vivo. Treatment of isolated hepatocytes with CDDO-Me directly stimulates AMPK activity and LKB1 phosphorylation and decreases acetyl-coA carboxylase activity; it also down-regulates lipogenic gene expression, suppresses gluconeogenesis, and increases glucose uptake. Inhibition of AMPK phosphorylation using compound C and lentiviral-mediated knockdown of AMPK completely blocks the CDDO-Me-induced effect on hepatocytes as well as C(2)C(12) cells. We conclude that the triterpenoid CDDO-Me has potent anti-diabetic action in diabetic mouse models that is mediated at least in part through AMPK activation. The in vivo anti-diabetogenic effects occur at a dose substantially lower than that used for anti-leukemia therapy. We suggest that CDDO-Me holds promise as a potential anti-diabetic agent.
Authors:
Pradip K Saha; Vasumathi T Reddy; Marina Konopleva; Michael Andreeff; Lawrence Chan
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-10-18
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  285     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-12-20     Completed Date:  2011-01-24     Revised Date:  2011-12-26    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  40581-92     Citation Subset:  IM    
Affiliation:
Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.
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MeSH Terms
Descriptor/Qualifier:
AMP-Activated Protein Kinases / genetics,  metabolism
Acetyl-CoA Carboxylase / genetics,  metabolism
Adipose Tissue / metabolism
Animals
Diabetes Mellitus, Experimental / blood,  drug therapy*,  genetics
Diet / adverse effects*
Enzyme Activation / drug effects,  genetics
Fatty Acids, Nonesterified / blood
Glucose / metabolism
Hypoglycemic Agents / pharmacology*,  therapeutic use
Insulin / blood
Mice
Mice, Mutant Strains
Muscle, Skeletal / metabolism
Oleanolic Acid / analogs & derivatives*,  pharmacology,  therapeutic use
Phosphorylation / drug effects,  genetics
Protein-Serine-Threonine Kinases / metabolism
Triglycerides / blood
Grant Support
ID/Acronym/Agency:
HL51586/HL/NHLBI NIH HHS; P30-DK079638/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Fatty Acids, Nonesterified; 0/Hypoglycemic Agents; 0/Insulin; 0/Triglycerides; 0/methyl 2-cyano-3,12-dioxoolean-1,9-dien-28-oate; 50-99-7/Glucose; 508-02-1/Oleanolic Acid; EC 2.7.1.-/Stk11 protein, mouse; EC 2.7.11.1/AMP-Activated Protein Kinases; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 6.4.1.2/Acetyl-CoA Carboxylase

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