Evidence map›Paper›PMID 38040681›Full record

ArticleNutrition & diabetes2023

Urolithin C alleviates pancreatic β-cell dysfunction in type 1 diabetes by activating Nrf2 signaling.

Cheng Luo, Can Hou, Danyi Yang, Tingting Tan, Chen Chao

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nutrition & diabetes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.3field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Nrf2 signaling pathway and its molecular regulatory mechanism.Journal of Zhejiang University. Science. B · 2026
    Review
  3. Review
  4. Review
  5. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Cheng LuoDepartment of Cardiovascular Surgery, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan Province, PR China.
Can HouNational Clinical Research Center for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan Province, PR China.
Danyi YangDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan Province, PR China.
Tingting TanDepartment of Immunology, School of Basic Medical Sciences, Central South University, Changsha, 410008, Hunan Province, PR China.
Chen ChaoNational Clinical Research Center for Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan Province, PR China. chaochen@csu.edu.cn.ORCID 0000-0002-5856-7881
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsType 1 diabetes (T1D) is an autoimmune disorder that destroys insulin-generating pancreatic β-cells. Preserving pancreatic β-cell function is important for treating T1D. Our study aims to explore the mechanism underlying urolithin C (UC)-mediated regulation of β-cell function.

methodsNon-obese diabetic (NOD) mice were administrated with UC to evaluate UC-mediated protection of T1D. The inflammation of the pancreas islets was examined by hematoxylin and eosin staining. Glucose-stimulated insulin secretion (GSIS) assay and oral glucose tolerance test were applied to evaluate the progression of T1D. MIN6 cells were treated with TNF-α, IL-1β and IFN-γ in the presence of UC. Cell viability was analyzed by CCK-8. Cell apoptosis, proliferation and DNA fragmentation were examined by Annexin V-FITC and PI staining, EdU incorporation and comet assays. Keap1, Nrf2, HO-1 and NQO1 were examined by western blot. Immunofluorescence staining was applied to detect Nrf2 and insulin.

resultsUC administration significantly reduced diabetes incidence, attenuated insulitis, elevated insulin levels and GSIS and reduced blood glucose and AUC in NOD mice. Cytokine treatment suppressed MIN6 cell viability and proliferation but enhanced apoptosis and DNA damage, and these detrimental effects were relieved by UC treatment. Furthermore, UC administration inhibited Keap1 expression and promoted the expression of Nrf2, HO-1 and NQO1 in NOD mice. Nrf2 signaling has been reported to be implicated in preventing the onset of diabetes, and HO-1 and NQO1 are phase II antioxidant enzymes that are regulated by Nrf2 signaling. Cytokine treatment upregulated Keap1 and downregulated Nrf2, HO-1 and NQO1 in MIN6 cells, but it was reversed by UC. The nuclear translocation of Nrf2 was prevented by cytokine treatment, but UC promoted its nuclear translocation. UC-mediated upregulation of Nrf2, HO-1 and NQO1, decreased cell apoptosis and increased proliferation and insulin secretion were abolished by silencing of Nrf2.

conclusionUC improves pancreatic β-cell function by activating Nrf2 signaling, thereby alleviating T1D progression.

Indexed as

Diabetes Mellitus, Type 1Insulin-Secreting CellsAnimalsCytokinesGlucoseHydrolyzable TanninsInsulinKelch-Like ECH-Associated Protein 1MiceMice, Inbred NODNF-E2-Related Factor 2Oxidative StressCytokinesGlucoseHydrolyzable TanninsInsulinKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2urolithin C

Identifiers

PMID38040681
PMCPMC10692094
OpenAlexW4389225644

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.