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dc.contributor.authorSreelekshmi, M-
dc.contributor.authorRaghu, K G-
dc.date.accessioned2023-01-31T08:46:11Z-
dc.date.available2023-01-31T08:46:11Z-
dc.date.issued2021-07-
dc.identifier.citationJournal of Biochemical and Molecular Toxicology;35(6):1-8en_US
dc.identifier.urihttps://doi.org/10.1002/jbt.22750-
dc.identifier.urihttp://localhost:8080/xmlui/handle/123456789/4239-
dc.description.abstractGlucokinase (GK), a key regulator of hepatic glucose metabolism in the liver and glucose sensor and mediator in the secretion of insulin in the pancreas, is not studied in detail for its therapeutic application in diabetes. Herein, we study the alteration in GK activity during hyperinsulinemia-induced insulin resistance in HepG2 cells. We also investigated the link between GK and Bcl-2-associated death receptor (BAD) during hyperinsulinemia. There are emerging demands for GK activators from natural resources, and we selected vanillic acid (VA) to evaluate its potential as GK activators during hyperinsulinemia in HepG2 cells. VA is a phenolic compound and a commonly used food additive in many food industries. We found that VA safeguarded GK inhibition during hyperinsulinemia significantly in HepG2 cells. VA also prevented the depletion of glycogen synthesis during hyperinsulinemia, which is evident from protein expression studies of phosphoenolpyruvate carboxykinase, glucose-6-phosphatase, glycogen synthase, and glycogen synthase kinase-3β. This was associated with activation of BAD activity, which was also confirmed by Western blotting. Molecular docking revealed strong binding between GK active site and VA, supporting their strong interaction. These are the first in vitro data to indicate the beneficial properties of VA with respect to insulin resistance induced by hyperinsulinemia by GK activation. Since it is activated via BAD, the hypoglycemia associated with general GK activation is not expected here and therefore has significant implications for future therapies against diabetes.en_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.subjectBADen_US
dc.subjectHepG2 cellsen_US
dc.subjectglucokinaseen_US
dc.subjectgluconeogenesisen_US
dc.subjecthyperinsulinemiaen_US
dc.titleVanillic Acid Mitigates the Impairments in Glucose Metabolism in HepG2 Cells Through BAD–GK Interaction During Hyperinsulinemiaen_US
dc.typeArticleen_US
Appears in Collections:2021

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