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- W1968900393 abstract "Antidiabetic drugs that activate the protein PPARγ had a bright start but soon lost their appeal because of undesirable side effects. Subtle modifications may once again make them suitable for treating diabetes. Thiazolidinedione antidiabetics such as rosiglitazone and pioglitazone are known to act through the nuclear receptor PPARγ, but some aspects of the mechanism of their insulin-sensitizing effect remain puzzling. Choi et al. now report that phosphorylation of PPARγ by Cdk5 is linked to obesity induced by high-fat feeding in mice. Several antidiabetic PPARγ ligands directly inhibit this action of Cdk5 on PPARγ, and thus support a more normal non-diabetic pattern of gene expression. In addition, inhibition of this PPARγ phosphorylation in humans by rosiglitazone is closely associated with its antidiabetic effects. This unusual pharmacology suggests a new model for a Cdk5–PPARγ link in the pathogenesis of obesity and diabetes, and for the therapeutic action of PPARγ ligands in these disorders as well as in metabolic syndrome, a combination of disorders that increases the risk of cardiovascular disease and diabetes." @default.
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- W1968900393 date "2010-07-01" @default.
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- W1968900393 title "New life for antidiabetic drugs" @default.
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- W1968900393 doi "https://doi.org/10.1038/466443a" @default.
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