Corrigendum to “Obesity in a model of gpx4 haploinsufficiency uncovers a causal role for lipid-derived aldehydes in human metabolic disease and cardiomyopathy” [Mol Metab 4 (6) (2015) 493–506]

Katunga, Lalage Adalaide; Gudimella, Preeti; Efird, Jimmy T.; Abernathy, Scott; Mattox, Taylor A.; Beatty, Cherese; Darden, Timothy M.; Thayne, Kathleen; Alwair, Hazaim; Kypson, Alan P.; Virag, Jitka A. I.; Anderson, Ethan J.

doi:10.1016/j.molmet.2015.06.005

Cited by 2 publications

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“…The systemic balance between oxidant and antioxidant levels is primarily regulated by the liver and might alter cardiac functions (40). Thus, we analyzed some fat-related serum biomarkers that are classically worsened by increasing lipid intake.…”

Section: Resultsmentioning

confidence: 99%

High-Fat and Fat-Enriched Diets Impair the Benefits of Moderate Physical Training in the Aorta and the Heart in Rats

et al. 2017

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AimMillions of people die each year due to cardiovascular disease (CVD). A Western lifestyle not only fuses a significant intake of fat with physical inactivity and obesity but also promotes CVD. Recent evidence suggests that dietary fat intake impairs the benefits of physical training. We investigated whether aerobic training could reverse the adverse effects of a high-fat diet (HFD) on the aorta. Then, we explored whether this type of exercise could reverse the damage to the heart that is imposed by fat-enriched diet (FED).MethodsRats were randomly assigned to two experiments, which lasted 8 weeks each. First, rats swam for 60 min and were fed either a regular diet [standard diet (STD)] or an HFD. After aortic samples had been collected, the rats underwent a histopathological analysis for different biomarkers. Another experiment subjected rats that were fed either an STD or an FED to swimming for 20 or 90 min.ResultsThe first experiment revealed that rats that were subjected to an HFD-endured increased oxidative damage in the aorta that exercises could not counteract. Together with increased cyclooxygenase 2 expression, an HFD in combination with physical training increased the number of macrophages. A reduction in collagen fibers with an increased number of positive α-actin cells and expression of matrix metalloproteinase-2 occurred concomitantly. Upon analyzing the second experiment, we found that physically training rats that were given an FED for 90 min/day decreased the cardiac adipose tissue density, although it did not protect the heart from fat-induced oxidative damage. Even though the physical training lowered cholesterol levels that were promoted by the FED, the levels were still higher than those in the animals that were given an STD. Feeding rats an FED impaired the swimming protocol’s effects on lowering triglyceride concentration. Additionally, exercise was unable to reverse the fat-induced deregulation in hepatic antioxidant and lipid peroxidation activities.ConclusionOur findings reveal that an increased intake of fat undermines the potential benefits of physical exercise on the heart and the aorta.

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Section: Resultsmentioning

confidence: 99%

High-Fat and Fat-Enriched Diets Impair the Benefits of Moderate Physical Training in the Aorta and the Heart in Rats

et al. 2017

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A Highly Sensitive, Reproducible Assay for Determining 4-hydroxynonenal Protein Adducts in Biological Material

Monroe¹,

Anderson

2019

BIO-PROTOCOL

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Oxidative stress is associated with numerous diseases, and markers of oxidative stress in biological material are becoming a mainstay of both experimental and clinical/epidemiological research.Lipid peroxidation is a major form of oxidative stress, but due to their rapid degradation and instability, lipid peroxides are notoriously difficult to measure, particularly in biological specimens where their production and removal are continuously occuring. Thus, a commonly used surrogate marker of lipid peroxidation is protein adducts of 4-Hydroxynonenal (HNE), an α, β-unsaturated hydroxyalkenal (i.e., a reactive aldehyde) formed via degradation of oxidized polyunsaturated fatty acids (PUFAs). HNE adducts can be measured via commercially-available immunosorbent assays, but these have their limitations due to excessive costs, and reproducibility among laboratories is challenging due to variability in assay sensitivity, procedure, and reagents. Here we present a reproducible, facile, and economically conservative protocol for quantifying HNE protein adducts. The key to this protocol is to generate HNEadduct standards by incubating bovine serum albumin (BSA) with HNE. These standards are then adsorbed to immunsorbent plastic in a multi-well plate format alongside biological samples. An enzymelinked immunosorbent assay (ELISA) is then performed on the multi-well plate using commerciallyavailable primary and secondary antibodies, and a peroxide-based fluorescent developing reagent. This protocol is highly sensitive and offers advantages to commercial sources in that it allows for reproducible, high-throughput quantitation of HNE adducts in a large number of samples.As such, it may be useful as a biomarker of chronic oxidative stress for experimental and clinical studies.

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Corrigendum to “Obesity in a model of gpx4 haploinsufficiency uncovers a causal role for lipid-derived aldehydes in human metabolic disease and cardiomyopathy” [Mol Metab 4 (6) (2015) 493–506]

Abstract: [This corrects the article DOI: 10.1016/j.molmet.2015.04.001.].

Cited by 2 publications

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High-Fat and Fat-Enriched Diets Impair the Benefits of Moderate Physical Training in the Aorta and the Heart in Rats

High-Fat and Fat-Enriched Diets Impair the Benefits of Moderate Physical Training in the Aorta and the Heart in Rats

A Highly Sensitive, Reproducible Assay for Determining 4-hydroxynonenal Protein Adducts in Biological Material

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