ArticleBiological trace element research2026
Zinc Deficiency Aggravates High-Fat Diet-Induced Renal Injury by Regulating Oxidative Stress and Inflammation via the Nrf2/HO-1 Pathway.
Article in Biological trace element research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Oxidative Stress as a Pathophysiological Core of Obesity: Preclinical Evidence for Antioxidant-Based Therapy Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Zinc, type 2 diabetes, diabetic kidney disease: focus on hypoxia.Frontiers in endocrinology · 2026Review
- Zinc deficiency predicts new-onset diabetic kidney disease in type 2 diabetes: a retrospective cohort study.Frontiers in nutrition · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
Obesity-related kidney disease (ORG) is associated with oxidative stress and inflammation. Zinc plays a crucial role in antioxidative defense, but its deficiency may exacerbate renal injury. The role of Zn deficiency in obesity-induced oxidative stress remains unclear. Male C57BL/6J mice were divided into four groups: ND/NZ (normal diet, normal Zn), ND/LZ (normal diet, low Zn), HFD/NZ (high-fat diet, normal Zn), and HFD/LZ (high-fat diet, low Zn) groups. After 24 weeks, renal function, histopathology, oxidative stress, and inflammatory markers were analyzed. The levels of ROS and key proteins in the Nrf2/HO-1 and PI3K/Akt pathways were assessed via Western blotting and immunofluorescence. An in vitro MPC5 podocyte model was used to examine the effects of Zn under palmitic acid stimulation, with siRNA-mediated Nrf2 knockdown. Zn deficiency exacerbated renal dysfunction, fibrosis, and inflammation in obese mice; increased ROS levels; suppressed Nrf2 signaling; and activated PI3K/Akt. In vitro, Zn supplementation reduced ROS levels and restored Nrf2 nuclear translocation, whereas Nrf2 knockdown aggravated oxidative stress. Zn deficiency promotes obesity-induced renal injury by increasing oxidative stress and inflammation through Nrf2 inhibition and PI3K/Akt activation.
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