Dataset Information

Metabolic Investigation on the Interaction Mechanism between Dietary Dihydrochalcone Intake and Lipid Peroxidation Product Acrolein Reduction.

ABSTRACT:

Scope

Acrolein (ACR), a lipid peroxidation product, pathologically participates in various chronic diseases. In vitro evidence suggestes that dietary dihydrochalcones (DHCs) potentiate safe and alternative therapeutics to synthetic pharmaceuticals for ACR scavenging. Here, to investigate whether ingested DHCs could trap ACR and thereof result in reductions in endogenous ACR in mice is aimed.

Methods and results

Three doses of phloretin (25, 100, and 400 mg kg^-1 ), a major dietary DHC, are orally administrated to mice and 24 h urine and fecal samples are collected, respectively. High-resolution MS-based targeted metabolomics reveal for the first time that phloretin and its oxidized metabolite are able to trap endogenous ACR via formation of ACR conjugates. Quantification further demonstrate that a) more than 13% of ingested phloretin can dose-dependently trap 0.77-9.92 nmol of ACR within 24 h; b) phloretin ingestion leads to marked reductions in both free ACR and ACR metabolites in mouse urine compared to control; and c) trapping reactions by phloretin can account for up to 20.1% of the total decreases in endogenous ACR, depending on the administration doses.

Conclusion

Findings from this study indicate that regular consumption of DHCs-rich diets holds great promise to alleviate the development of ACR-associated chronic diseases.

SUBMITTER: Zhu Y

PROVIDER: S-EPMC9081224 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature

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Publications

Metabolic Investigation on the Interaction Mechanism between Dietary Dihydrochalcone Intake and Lipid Peroxidation Product Acrolein Reduction.

Zhu Yingdong Y Wang Weixin W Huang Qiju Q Hu Changlin C Sang Shengmin S

Molecular nutrition & food research 20220303 9

<h4>Scope</h4>Acrolein (ACR), a lipid peroxidation product, pathologically participates in various chronic diseases. In vitro evidence suggestes that dietary dihydrochalcones (DHCs) potentiate safe and alternative therapeutics to synthetic pharmaceuticals for ACR scavenging. Here, to investigate whether ingested DHCs could trap ACR and thereof result in reductions in endogenous ACR in mice is aimed.<h4>Methods and results</h4>Three doses of phloretin (25, 100, and 400 mg kg<sup>-1</sup> ), a maj ...[more]

PMID: 35194934

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Project description:BackgroundHigh glycemic index (GI) diets have been linked to elevated risk of cardiometabolic diseases. One possible underlying mechanism comes from high GI diet's potential to promote lipid peroxidation.ObjectivesWe aim to evaluate whether and to what extent dietary carbohydrate quality and quantity are associated with systemic levels of lipid peroxidation in females.MethodsIn this cross-sectional analysis of 2163 middle-aged women, a subset of the Shanghai Women's Health Study, we measured lipid peroxidation biomarkers F2-isoprostanes (F2-IsoPs) and its metabolite, 2,3-dinor-5,6-dihydro-15-F2t-IsoP (F2-IsoP-M), in urine. The quality of carbohydrate was defined by dietary GI, assessed using a validated FFQ via in-person interviews. A multivariable linear regression model with restricted cubic spline functions was used to evaluate the association of measured biomarkers with carbohydrate intake and dietary GI.ResultsAfter adjustment for potential confounding factors such as cigarette smoking, BMI, and comorbidities, among others, we found that F2-IsoP-M concentrations were positively associated with both carbohydrate intake and dietary GI. Carbohydrate intake and dietary GI were weakly correlated (r = 0.12). When further mutually adjusted for the 2 factors, the positive association with F2-IsoP-M remained statistically significant for GI (P = 0.004) but not for carbohydrate intake (P = 0.50). Compared with those in the 10th percentile of dietary GI, fold increases (95% CI) in F2-IsoP-M concentrations for those in the 30th, 50th, 70th, and 90th percentiles were 1.03 (1.00, 1.07), 1.06 (1.01, 1.10), 1.09 (1.03, 1.14), and 1.13 (1.05, 1.21), respectively. Moreover, there appeared a threshold regarding the association between dietary GI and F2-IsoP-M concentrations, with the dose-effect slope of GI being 2.3 times greater when GI was ≥75 relative to GI <75.ConclusionsThis study provides evidence that the quality of dietary carbohydrate may be more important than the quantity of the intake with regard to systemic lipid peroxidation.

Dataset Information

Metabolic Investigation on the Interaction Mechanism between Dietary Dihydrochalcone Intake and Lipid Peroxidation Product Acrolein Reduction.

Scope

Methods and results

Conclusion

Publications

Metabolic Investigation on the Interaction Mechanism between Dietary Dihydrochalcone Intake and Lipid Peroxidation Product Acrolein Reduction.

Similar Datasets

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