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Objective: To examine if peroxiredoxin 2 (Prx2) deficiency aggravates high-fat diet-induced insulin resistance.
Material And Methods: Insulin sensitivity was measured in Prx2 knockout (KO) and wild-type (WT) littermates using the hyperinsulinemic-euglycemic clamp.
Results: Whole body glucose turnover, glucose uptake, and levels of glucose transporter 4 (Glut4) protein in the skeletal muscle were found to be lower. This was followed by increased expression of oxidative stress markers in Prx2 KO mice than that in WT mice in the control diet group. Although, a 12-week high-fat diet induced insulin resistance and enhanced oxidative stress in both genotypes, there was no difference between WT and Prx2 KO mice with respect to insulin sensitivity and the level of oxidative stress markers. Accordingly, the levels of phosphorylated Akt and Glut4 were similar between the two genotypes.
Conclusion: These results suggest that Prx2 does not affect high-fat diet-induced oxidative stress and insulin resistance in mice.
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http://dx.doi.org/10.1080/13813455.2020.1733026 | DOI Listing |
J Trace Elem Med Biol
September 2025
Department of Neurology, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, China. Electronic address:
Objective: We previously documented that exposure to a spectrum of elements is associated with autism spectrum disorder (ASD). However, there is a lack of mechanistic understanding as to how elemental mixtures contribute to the ASD development.
Materials And Methods: Serum and urinary concentrations of 26 elements and six biomarkers of ASD-relevant pathophysiologic pathways including serum HIPK 2, serum p53 protein, urine malondialdehyde (MDA), urine 8-OHdG, serum melatonin, and urine carnitine, were measured in 21 ASD cases and 21 age-matched healthy controls of children aged 6-12 years.
Mol Pharm
September 2025
Affiliated Hospital of Shandong Second Medical University, Shandong Second Medical University, Weifang 261053, Shandong, P. R. China.
Myocardial injury constitutes a life-threatening complication of sepsis, driven by synergistic oxidative-inflammatory pathology involving dysregulated production of reactive oxygen species (ROS), reactive nitrogen species (RNS), and proinflammatory cytokines. This pathophysiological cascade remarkably elevates morbidity and mortality rates in septic patients, emerging as a key contributor to poor clinical outcomes. Despite its clinical significance, no clinically validated therapeutics currently exist for managing septic cardiomyopathy.
View Article and Find Full Text PDFPol Merkur Lekarski
September 2025
I. HORBACHEVSKY TERNOPIL NATIONAL MEDICAL UNIVERSITY, TERNOPIL, UKRAINE.
Objective: Aim: To evaluate the state of oxidation processes and morphological changes in the heart of rats with chronic hypodynamia during the development of epinephrine heart damage (EHD)..
Patients And Methods: Materials and Methods: The study was performed on 144 white male Wistar rats.
Exp Physiol
September 2025
Department of Hepatobiliary Surgery, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, China.
Hepatic ischaemia-reperfusion (IR) injury is a serious clinical issue, especially in patients with type 2 diabetes mellitus (T2DM). As mitochondria play a critical role in the regulation of IR-induced liver damage, mitochondria-targeted treatment is of the utmost significance for improving outcomes. The present study explored the mitoprotective role of combined ginsenoside-MC1 (GMC1) and irisin administration in diabetic rats with hepatic IR injury.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Cardiac Surgery, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Background: Cardiac ischemia reperfusion (I/R) injury is a serious consequence of reperfusion therapy for myocardial infarction (MI). Peptidylarginine deiminase 4 (PAD4) is a calcium-dependent enzyme that catalyzes the citrullination of proteins. In previous studies, PAD4 inhibition protected distinct organs from I/R injury by preventing the formation of neutrophil extracellular traps (NETs) and attenuating inflammatory responses.
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