ArticleDiabetes2014
Glutathionylated lipid aldehydes are products of adipocyte oxidative stress and activators of macrophage inflammation.
Article in Diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 57 citations in OpenAlex.
- High-Protein Intake during Weight Loss Therapy Eliminates the Weight-Loss-Induced Improvement in Insulin Action in Obese Postmenopausal Women.Cell reports · 2016Trial
- Oxidative Stress as a Pathophysiological Core of Obesity: Preclinical Evidence for Antioxidant-Based Therapy Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- 4-Hydroxynonenal, a Potential Biomarker for Lung Inflammatory Diseases.International journal of molecular sciences · 2026Review
- Chchd10: A Novel Metabolic Sensor Modulating Adipose Tissue Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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- Neutron encoded derivatization of endothelial cell lysates for quantitation of aldehyde metabolites using nESI-LC-HRMS.Analytica chimica acta · 2022Article
- Anticancer Activity of Ω-6 Fatty Acids through Increased 4-HNE in Breast Cancer Cells.Cancers · 2021Article
- In Search for Multi-Target Ligands as Potential Agents for Diabetes Mellitus and Its Complications-A Structure-Activity Relationship Study on Inhibitors of Aldose Reductase and Protein Tyrosine Phosphatase 1B.Molecules (Basel, Switzerland) · 2021Article
- Aerobic Exercise in the Management of Metabolic Dysfunction Associated Fatty Liver Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Review
- Comparative Transcriptome Profiling of Cold Exposure and β3-AR Agonist CL316,243-Induced Browning of White Fat.Frontiers in physiology · 2021Article
- Intra-site differential inhibition of multi-specific enzymes.Journal of enzyme inhibition and medicinal chemistry · 2020Review
- Aldose Reductase Differential Inhibitors in Green Tea.Biomolecules · 2020Article
- Nicotine exposure increases markers of oxidant stress in stored red blood cells from healthy donor volunteers.Transfusion · 2020Article
- Stereoselectivity of Aldose Reductase in the Reduction of Glutathionyl-Hydroxynonanal Adduct.Antioxidants (Basel, Switzerland) · 2019Article
- Adipose oxidative stress and protein carbonylation.The Journal of biological chemistry · 2019Review
- A carnosine analog mitigates metabolic disorders of obesity by reducing carbonyl stress.The Journal of clinical investigation · 2018Article
- Obesity-induced protein carbonylation in murine adipose tissue regulates the DNA-binding domain of nuclear zinc finger proteins.The Journal of biological chemistry · 2018Article
- The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis.The Journal of clinical investigation · 2017Review
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Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Obesity-induced insulin resistance has been linked to adipose tissue lipid aldehyde production and protein carbonylation. Trans-4-hydroxy-2-nonenal (4-HNE) is the most abundant lipid aldehyde in murine adipose tissue and is metabolized by glutathione S-transferase A4 (GSTA4), producing glutathionyl-HNE (GS-HNE) and its metabolite glutathionyl-1,4-dihydroxynonene (GS-DHN). The objective of this study was to evaluate adipocyte production of GS-HNE and GS-DHN and their effect on macrophage inflammation. Compared with lean controls, GS-HNE and GS-DHN were more abundant in visceral adipose tissue of ob/ob mice and diet-induced obese, insulin-resistant mice. High glucose and oxidative stress induced production of GS-HNE and GS-DHN by 3T3-L1 adipocytes in a GSTA4-dependent manner, and both glutathionylated metabolites induced secretion of tumor necrosis factor-α from RAW 264.7 and primary peritoneal macrophages. Targeted microarray analysis revealed GS-HNE and GS-DHN induced expression of inflammatory genes, including C3, C4b, c-Fos, igtb2, Nfkb1, and Nos2. Transgenic overexpression of GSTA4 in mouse adipose tissue led to increased production of GS-HNE associated with higher fasting glucose levels and moderately impaired glucose tolerance. These results indicated adipocyte oxidative stress results in GSTA4-dependent production of proinflammatory glutathione metabolites, GS-HNE and GS-DHN, which may represent a novel mechanism by which adipocyte dysfunction results in tissue inflammation and insulin resistance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.