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Diabetes is a metabolic and chronic disease affecting different tissues' metabolism. Genetic factors, lifestyles, and dietary habits can cause it. In diabetes, oxidative stress can occur in metabolic disorders, negatively affecting it. The antioxidants are essential in reducing or completely stopping the harmful effects of these adverse effects on the tissues. In the present study, we aimed to determine the combined effects of lipoic acid, vitamin E, and selenium in the kidneys of diabetic mice. For this experiment, the Balb/c mice were used and divided into five groups: citrate buffer, the solvents of the antioxidants, combined the antioxidants (α-lipoic acid, vitamin E, and selenium), streptozotocin, combined with the antioxidants and streptozotocin (A+D). At the end of 30 days of this process, the mice were sacrificed by cervical dislocation. Kidney tissues were taken for morphological, Western blotting, and biochemical analyses. The tissue was used for staining with Masson's trichrome and periodic acid-Schiff (PAS) of renal tissue sections taken for histological analysis; Western blotting such as the level of IL-10, IL-1β, TGF-β, p38, cCas3, NRF2; biochemical parameters such as the level of GSH, LPO, SOD, CAT, GR, TAS, TOS, ROS, OSI, PON, CA, LDH, AR, ADA, arginase, OH-proline, and AOPP. The histological findings showed mild damage to the kidney tissue of diabetic mice. Western blot results showed that the damage was independent of inflammation. Biochemical results revealed that administering combined antioxidants to diabetic mice protects the kidney tissue.
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http://dx.doi.org/10.1111/1750-3841.70544 | DOI Listing |
JCI Insight
September 2025
Diabetes & Metabolism Research Center, University of Utah, Salt Lake City, United States of America.
Impaired muscle regrowth in aging is underpinned by reduced pro-inflammatory macrophage function and subsequently impaired muscle cellular remodeling. Macrophage phenotype is metabolically controlled through TCA intermediate accumulation and activation of HIF1A. We hypothesized that transient hypoxia following disuse in old mice would enhance macrophage metabolic inflammatory function thereby improving muscle cellular remodeling and recovery.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Department of Medicine, Institute for Transformative Molecular Medicine, Case Western Reserve University School of Medicine, Cleveland, OH 44106.
The β-adrenergic receptor (βAR), a prototype G protein-coupled receptor, controls cardiopulmonary function underpinning O delivery. Abundance of the βAR is canonically regulated by G protein-coupled receptor kinases and β-arrestins, but neither controls constitutive receptor levels, which are dependent on ambient O. Basal βAR expression is instead regulated by the prolyl hydroxylase/pVHL-E3 ubiquitin ligase system, explaining O responsivity.
View Article and Find Full Text PDFMetabolomics
September 2025
Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK.
Introduction: Knockout of the Fmo5 gene in mice led to a lean, slow-ageing phenotype characterised by the presence of 2,3-butanediol isomers in their urine and plasma. Oral treatment of wildtype mice with 2,3-butanediol led to a low cholesterol, low epididymal fat phenotype.
Objectives: Determine if significant, heterozygous coding variations in human FMO5 would give rise to similar clinical and metabolic phenotypes in humans, as in C57BL/6J mice with knockout of the Fmo5 gene and in particular, increased excretion of 2,3-butanediol.
Diabetologia
September 2025
Walther Straub Institute of Pharmacology and Toxicology, LMU Munich, Munich, Germany.
Aims/hypothesis: Unimolecular peptides targeting the receptors for glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and glucagon (GCG) have been shown to improve glycaemic management in both mice and humans. Yet the identity of the downstream signalling events mediated by these peptides remain to be elucidated. Here, we aimed to assess the mechanisms by which a validated peptide triagonist for GLP-1/GIP/GCG receptors (IUB447) stimulates insulin secretion in murine pancreatic islets.
View Article and Find Full Text PDFBackground: Diabetes mellitus is still a major health problem affecting individuals all over the world. Type 1 diabetes mellitus occurs due to insulin deficiency resulting from the destruction of pancreatic β-cells. This study aimed to investigate how vitamin D reduces blood glucose levels and HbA1c.
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