Loss and Recovery of Glutaredoxin 5 Is Inducible by Diet in a Murine Model of Diabesity and Mediated by Free Fatty Acids In Vitro

Petry, Sebastian Friedrich; Römer, Axel; Rawat, Divya; Brunner, Lara; Lerch, Nina; Zhou, Mengmeng; Grewal, Rekha; Sharifpanah, Fatemeh; Sauer, Heinrich; Eckert, Gunter P.; Linn, Thomas

doi:10.3390/antiox11040788

Cited by 3 publications

(1 citation statement)

References 61 publications

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“…Because obese individuals are in a high-fat state, the increase of free fatty acid content in this state causes insulin resistance and reduces the number of pancreatic β-cells by apoptosis, leading to abnormal insulin secretion and decreased expression of insulin-receptor-related proteins. This phenomenon is called lipotoxicity [ 4 , 5 ]. Lipotoxicity is related to inflammation and oxidative stress; it not only acts through some metabolic pathways but also affects some protein receptor pathways in cells [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Spore Oil-Functionalized Selenium Nanoparticles Protect Pancreatic Beta Cells from Palmitic Acid-Induced Apoptosis via Inhibition of Oxidative Stress-Mediated Apoptotic Pathways

et al. 2023

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Oxidative stress damage of pancreatic β-cells is a key link in the pathogenesis of type 2 diabetes mellitus. A long-term increase of free fatty acids induces the increase of reactive oxygen species (ROS) in β-cells, leading to apoptosis and dysfunction of β-cells. Ganoderma lucidum spore oil (GLSO) is a functional food complex with strong antioxidant activity, but its solubility and stability are poor. In the present study, GLSO-functionalized selenium nanoparticles (GLSO@SeNPs) with high stability and uniform particle size were synthesized by a high-pressure homogeneous emulsification method. The aim of this study was to investigate the protective effects of GLSO@SeNPs on INS-1E rat insulinoma β-cells against palmitic-acid (PA)-induced cell death, as well as the underlying mechanisms. Our results showed that GLSO@SeNPs had good stability and biocompatibility, and they significantly inhibited the PA-induced apoptosis of INS-1E pancreatic cells by regulating the activity of related antioxidant enzymes, including thioredoxin reductase (TrxR), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Western blot analysis showed that GLSO@SeNPs reversed the PA-induced changes in MAPK pathway protein expression levels. Thus, the present findings provided a new theoretical basis for utilizing GLSO@SeNPs as a treatment for type 2 diabetes.

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Section: Introductionmentioning

confidence: 99%

Spore Oil-Functionalized Selenium Nanoparticles Protect Pancreatic Beta Cells from Palmitic Acid-Induced Apoptosis via Inhibition of Oxidative Stress-Mediated Apoptotic Pathways

et al. 2023

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The significance of glutaredoxins for diabetes mellitus and its complications

Zhou,

Hanschmann,

Römer

et al. 2024

Redox Biology

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The mechanism of ferroptosis and its related diseases

Feng,

Tang,

Wang

et al. 2023

Mol Biomed

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Ferroptosis, a regulated form of cellular death characterized by the iron-mediated accumulation of lipid peroxides, provides a novel avenue for delving into the intersection of cellular metabolism, oxidative stress, and disease pathology. We have witnessed a mounting fascination with ferroptosis, attributed to its pivotal roles across diverse physiological and pathological conditions including developmental processes, metabolic dynamics, oncogenic pathways, neurodegenerative cascades, and traumatic tissue injuries. By unraveling the intricate underpinnings of the molecular machinery, pivotal contributors, intricate signaling conduits, and regulatory networks governing ferroptosis, researchers aim to bridge the gap between the intricacies of this unique mode of cellular death and its multifaceted implications for health and disease. In light of the rapidly advancing landscape of ferroptosis research, we present a comprehensive review aiming at the extensive implications of ferroptosis in the origins and progress of human diseases. This review concludes with a careful analysis of potential treatment approaches carefully designed to either inhibit or promote ferroptosis. Additionally, we have succinctly summarized the potential therapeutic targets and compounds that hold promise in targeting ferroptosis within various diseases. This pivotal facet underscores the burgeoning possibilities for manipulating ferroptosis as a therapeutic strategy. In summary, this review enriched the insights of both investigators and practitioners, while fostering an elevated comprehension of ferroptosis and its latent translational utilities. By revealing the basic processes and investigating treatment possibilities, this review provides a crucial resource for scientists and medical practitioners, aiding in a deep understanding of ferroptosis and its effects in various disease situations.

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Loss and Recovery of Glutaredoxin 5 Is Inducible by Diet in a Murine Model of Diabesity and Mediated by Free Fatty Acids In Vitro

Cited by 3 publications

References 61 publications

Spore Oil-Functionalized Selenium Nanoparticles Protect Pancreatic Beta Cells from Palmitic Acid-Induced Apoptosis via Inhibition of Oxidative Stress-Mediated Apoptotic Pathways

Spore Oil-Functionalized Selenium Nanoparticles Protect Pancreatic Beta Cells from Palmitic Acid-Induced Apoptosis via Inhibition of Oxidative Stress-Mediated Apoptotic Pathways

The significance of glutaredoxins for diabetes mellitus and its complications

The mechanism of ferroptosis and its related diseases

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