XXXX activates key components of insulin signaling pathway mimicking insulin activity.

@entity1 @entity10175 @entity563 @entity6 @entity7425 @entity209 @entity8277 @entity413 @entity2368 @entity164 @entity65 @entity4211 @entity4901 @entity860 @entity1889 @entity4149 @entity4854 @entity16074
SCOPE: Insulin resistance represents an independent risk factor for metabolic and @entity65 . Researchers have been interested in identifying active harmless compounds, as many insulin-sensitizing drugs have shown unwanted side-effects. It has been demonstrated that @entity4211 and one of their representative metabolites, @entity16074 ( @entity4901 ), ameliorate @entity4854 , and insulin sensitivity. This study investigated the mechanism of action of @entity4901 responsible for the @entity413 uptake upregulation. METHODS AND RESULTS: In @entity1 visceral adipocytes, @entity4901 stimulated @entity10175 ( @entity10175 ) @entity4149 phosphorylation (+40% with respect to untreated cells) and the downstream events, i.e. @entity7425 3-kinase binding to @entity10175 and Akt phosphorylation (+100%, +180%, respectively, with respect to untreated cells). The insulin-like activity of @entity4901 seemed to be mediated by @entity8277 since by inhibiting its autophosphorylation, the @entity4901 effects were completely abolished. Furthermore, @entity4901 was able to activate @entity860 -activated protein kinase, a @entity563 / @entity1889 kinase whose activation elicits insulin-sensitizing effects. CONCLUSION: This study showed that @entity4901 stimulates the insulin signaling pathway in @entity1 adipocytes increasing @entity2368 translocation and @entity413 uptake. Decreasing insulin resistance is a most desirable aim to be reached for an effective therapeutic/preventive action against @entity209 and @entity164 2 @entity6 . Identifying specific food/food components able to improve @entity413 metabolism can offer an attractive, novel, and economical strategy.
