X-3, a @entity15791 derivative, stimulates XXXX -activated protein kinase and reduces hyperglycemia and obesity in db/db @entity19 .

@entity137 @entity15791 @entity6625 @entity6 @entity19 @entity2448 @entity1674 @entity860 @entity204 @entity413 @entity2449
UNASSIGNED: @entity6 is a major health concern, affecting nearly 10% of the population. Here we describe a potential novel therapeutic agent for this disease, X-3, a derivative of @entity15791 . Therapeutic administration of X-3 significantly and dose-dependently reduced plasma @entity413 and @entity1674 in db/db @entity19 following 8 week-treatments. Treatment with X-3 dose-dependently increased the number of insulin-positive b-cell mass. Importantly, X-3 did not cause any @entity204 or signs of @entity137 in acute @entity137 studies. Study of mechanism of action revealed that X-3 increased @entity413 uptake in parallel with increased phosphorylation of @entity860 -activated protein kinase (AMPK) in 3T3-L1 cells. It activates AMPK in both @entity2448 -dependent and -independent manner. Furthermore, administration of X-3 resulted in activation of AMPK and its downstream target, @entity6625 carboxylase (ACC) in the hypothalamus, liver, muscle and adipose tissues of C57BL/6 @entity19 . An 80   mg/kg X-3 was more potent than @entity2449 at 500   mg/kg in the hypothalamus, and interscapular fat tissues, potent than MF at the same dose in the liver. Thus, we conclude that X-3 is a promising new class of AMPK activating drug, and can potentially be used in the treatment of type 2 @entity6 .
