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Elevated resistin levels activate the c-Jun N-terminal kinase (JNK) pathway, which phosphorylates IRS-1 at serine residues, impairing its function and resulting in reduced glucose uptake and heightened insulin resistance ( In a recent investigation involving insulin-resistant rats subjected to a high-fat diet (Wang X

Of note, consistent with post-translational mTOR inhibition by rapamycin, MYC was significantly upregulated, yet MYC targets were significantly downregulated (Fig

No one has tested whether the effects are additive, synergistic, or negligible when combined

HSA, human serum albumin