ArticleInternational journal of molecular sciences2025
Erythropoietin Attenuates Insulin Resistance and Renal Inflammation in High-Sucrose-Treated Rats.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Hepatocyte hedgehog signaling controls ferroptosis to alleviate aging-related organ dysfunction.JCI insight · 2026Article
- Chasing the FoxO in Metabolic Disorders: Novel Considerations for Oxidative Stress, Programmed Cell Death, Wnt, and the Gut Microbiome.Antioxidants (Basel, Switzerland) · 2026Review
- Osteoarthritis and dementia: contrasting disorders driven by mutual pathways of autophagy, mTOR, GLP-1, AMPK, Wnt, and WISP1.Expert review of clinical pharmacology · 2026Review
- Running out the clock: Circadian rhythm dysfunction in cognitive disease.International review of neurobiology · 2026Review
- Exploring the Role of SPARC in Atherosclerosis: Mechanisms and Potential Implications.Current atherosclerosis reports · 2025Review
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Authors and funding
5 authors.
Funding
Abstract
Erythropoietin (EPO), clinically used as a therapeutic agent for patients with renal anemia, has been reported to exert tissue protective effects independently of hematopoiesis. Insulin resistance is a pathophysiological condition that causes hypertension, diabetes mellitus, and dyslipidemia, leading to vascular and renal injury. The present study investigated whether EPO would improve insulin resistance and vascular and renal injury in chronic sucrose treatment-induced insulin resistant model rats. Sucrose (12%) was given in drinking water for 10 weeks to induce insulin resistance, and EPO (75 U/kg, 3 times/week) was administered subcutaneously for the last 4 weeks. Responses to the oral glucose tolerance test and values of the homeostatic model assessment for insulin resistance indicated that EPO improved insulin resistance in sucrose-treated rats. Though there were no differences in the expression of phospho-Akt (Ser473)/total Akt among all groups, EPO increased that of phospho-STAT3 (Tyr705)/total STAT3 in the liver. Macrophage infiltration into the adventitial area of the aorta and renal overexpression of monocyte chemoattractant protein-1 in the sucrose-treated group were suppressed by EPO treatment, suggesting anti-inflammatory effects of EPO. EPO also decreased collagen I expression in the kidney. A proinflammatory M1-type macrophage marker, tumor necrosis factor-α, was decreased, and anti-inflammatory M2-type macrophage markers, arginase-1 and interleukin-10, were increased by EPO treatment. These results suggest that EPO improved insulin resistance and vascular and renal inflammation in the setting of insulin resistance.
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