2026-10-19T01:02:07Zhttps://ebyu-rdlopen.rawdatalibrary.net/oai/request

oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/101432026-10-18T21:13:09Zopenairedrivercom_ebyu_10000col_ebyu_10001

Sulforaphane Against the Metabolic Consequences of a High-Glycemic-Index Diet: Protective and Therapeutic Mechanisms Associated with Obesity and Insulin ResistanceÇubuk, MihricanPınar, Aylin AçıkgözSüleyman, BahadırTaş, Necip Gökhanbioactive compoundsdyslipidemiafunctional foodglycemic controlglycemic indexinsulin resistancemolecular mechanismsobesitysulforaphaneAdiponectinAnimalsBlood GlucoseDietDietary SupplementsDyslipidemiasGlycated HemoglobinInsulinInsulin Receptor Substrate ProteinsIsothiocyanatesMaleMiceMice, Inbred C57BLSulfoxidesWeight Gainglucosehemoglobin A1cmessenger RNAperoxisome proliferator activated receptor gamma coactivator 1alphasirtuin 1sirtuin 3Objective: This study investigated the effects of different doses and timing of sulforaphane (SFN) supplementation on reducing obesity induced by a high-glycemic-index diet (HGID) and on correcting poor glycemic control and dyslipidemia in C57BL/6 mice. Method: For 15 weeks, mice were administered a control diet (control), HGID, HGID + oral 5 mg/kg/day SFN (HGID + LSFN), or HGID + 20 mg/kg/day SFN (HGID + HSFN), and following 15 weeks of HGID, mice were treated with 5 mg/kg/day SFN (PO-HGID + LSFN) or 20 mg/kg/day SFN (PO-HGID + HSFN) for 5 weeks. Results: SFN reduced body weight gain and serum glucose. The lowest levels of HbA1c were observed in the control and HGID + LSFN groups. Mice in the HGID group exhibited impaired glucose clearance and were less sensitive to insulin compared to the control. A remarkable improvement in glucose and insulin tolerance was observed in both PO-HGID + SFN and HGID + SFN groups. Lipid profile parameters and serum insulin levels were found to be lower in the control and HGID + SFN groups compared to the HGID group. SFN increased serum adiponectin levels when administered concurrently with HGID. IRS1 and IRS2 levels were highest in the control and HGID + LSFN groups, and high-dose SFN supplementation suppressed IRS1 independently of timing. Exposure to HGID downregulated the expression of PGC-1α and sirtuins. SIRT1 and SIRT3 gene expressions showed a significant increase at both doses, whereas SIRT2 gene expression increased significantly only at 5 mg/kg/day SFN. FASN expression was upregulated in all HGID-fed groups with or without SFN intervention. Conclusions: SFN may reverse the adverse effects of HGID in a time- and dose-dependent manner by regulating postprandial insulin, inhibiting gluconeogenesis, and enhancing fatty acid oxidation through the activation of sirtuins and PGC-1α. © 2026 by the authors.Multidisciplinary Digital Publishing Institute (MDPI)2026Articlehttps://rdlopen.rawdatalibrary.net/r/ebyu/10143https://doi.org/10.3390/nu180405742072-6643enNutrientsinfo:eu-repo/semantics/openAccessinfo:eu-repo/semantics/articlehttps://ebyu-rdlopen.rawdatalibrary.net/tr/items/ebyu/10143