N-Acetylneuraminic Acid Supplementation Prevents High Fat Diet-Induced Insulin Resistance in Rats through Transcriptional and Nontranscriptional Mechanisms

<div>Proposed schematic showing targets of SA transcriptional regulation of insulin signaling pathway. SA prevents insulin resistance in HFD-fed rats by influencing the transcriptional regulation of multiple genes. Gck: glucokinase; I<i>κ</i>bk<i>β</i>: inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase beta; IRS: insulin receptor substrate; KCNJ11: potassium inwardly rectifying channel, subfamily J, member 11; Mapk: mitogen-activated protein kinase; mTOR: mammalian target of rapamycin; Pi3k: phosphoinositide-3-kinase; Pk: pyruvate kinase; and Prkcz: protein kinase C, zeta.</div>

BioMed Research International

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Figure 5

Figure 5: N-Acetylneuraminic Acid Supplementation Prevents High Fat Diet-Induced Insulin Resistance in Rats through Transcriptional and Nontranscriptional Mechanisms 

Figure 5 | N-Acetylneuraminic Acid Supplementation Prevents High Fat Diet-Induced Insulin Resistance in Rats through Transcriptional and Nontranscriptional Mechanisms 