Pseudoginsenoside F11 acts as a novel partial PPARγ agonist in vitro, suggesting potential for development as a type 2 diabetes therapeutic with potentially fewer side effects than full agonists.
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p-F11 merits preclinical optimization as partial PPARγ agonist; leaves open therapeutic potential in type 2 diabetes pending human studies.
PPAR γ is a nuclear hormone receptor that functions as a master regulator of adipocyte differentiation and development. Full PPAR γ agonists, such as the thiazolidinediones (TZDs), have been widely used to treat type 2 diabetes. However, they are characterized by undesirable side effects due to their strong agonist activities. Pseudoginsenoside F11 (p-F11) is an ocotillol-type ginsenoside isolated from Panax quinquefolium L. (American ginseng). In this study, we found that p-F11 activates PPAR γ with modest adipogenic activity. In addition, p-F11 promotes adiponectin oligomerization and secretion in 3T3-L1 adipocytes. We also found that p-F11 inhibits obesity-linked phosphorylation of PPAR γ at Ser-273 by Cdk5. Therefore, p-F11 is a novel partial PPAR γ agonist, which might have the potential to be developed as a new PPAR γ -targeted therapeutics for type 2 diabetes.
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Wu et al. (2013) studied this question.
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