ArticleEndocrinology, diabetes & metabolism2020
Autocrine C-peptide protects INS1 β cells against palmitic acid-induced oxidative stress in peroxisomes by inducing catalase.
Article in Endocrinology, diabetes & metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The trial behind it
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Association between free triiodothyronine, resting metabolic rate, systemic immune-inflammation index levels and diabetic retinopathy in type 2 diabetic patients with euthyroidism.Frontiers in endocrinology · 2026Article
- Protective effects of Stevia rebaudiana extracts on beta cells in lipotoxic conditions.Acta diabetologica · 2022Article
- Insulin Requirement and Complications Associated With Serum C-Peptide Decline in Patients With Type 1 Diabetes Mellitus During 15 Years After Diagnosis.Frontiers in endocrinology · 2022Article
- Fatty Acids Metabolism: The Bridge Between Ferroptosis and Ionizing Radiation.Frontiers in cell and developmental biology · 2021Review
- Autocrine C-peptide protects INS1 β cells against palmitic acid-induced oxidative stress in peroxisomes by inducing catalase.Endocrinology, diabetes & metabolism · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
aimsC-peptide, produced by pancreatic β cells and co-secreted in the bloodstream with insulin, has antioxidant properties in glucose- and hydrogen peroxide (H MATERIALS AND
methodsWe exposed INS1 β cells to palmitic acid and C-peptide in the setting of increasing glucose concentration and tested for changes in parameters of stress and death. To study the ability of C-peptide to lower peroxisomal H
resultsC-peptide protects INS1 β cells from the combined effect of palmitic acid and glucose by reducing peroxisomal H
conclusionsIn conditions of glucolipotoxicity, C-peptide increases catalase expression and reduces peroxisomal oxidative stress and death of INS1 β cells. Maintenance of C-peptide secretion is a pro-survival requisite for β cells in adverse conditions. Loss of C-peptide secretion would render β cells more vulnerable to stress and death leading to secretory dysfunction and diabetes.
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Registered trials
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