Evidence map›Paper›PMID 41593307›Full record

ArticleExperimental & molecular medicine2026

Impaired insulin secretion via the Wnt5a/β-catenin pathway contributes to diabetes development in pancreatic cancer.

Minyoung Lee, Ho Seon Park, Hyung Sun Kim, ARim Choi, Ji Hae Nahm, Beom Jin Lim, Jong Suk Park, Chul Woo Ahn, Younhee Ko, Dong Ki Lee and 3 more

Abstract read
In one paragraph

Article in Experimental & molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

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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

1 citing paper in PubMed.

  1. Article
4 · The record

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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

13 authors.

Minyoung Lee *Department of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea.
Ho Seon Park *Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
Hyung Sun KimDepartment of Surgery, Pancreatobiliary Cancer Clinic, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
ARim ChoiDepartment of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
Ji Hae NahmDepartment of Pathology, Gangnam Severance Hospital, Seoul, South Korea.
Beom Jin LimDepartment of Pathology, Gangnam Severance Hospital, Seoul, South Korea.
Jong Suk ParkDepartment of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
Chul Woo AhnDepartment of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
Younhee KoDivision of Biomedical Engineering, Hankuk University of Foreign Studies, Gyeonggi-do, South Korea.
Dong Ki LeeDepartment of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.ORCID http://orcid.org/0000-0002-0048-9112
Dong Sup YoonDepartment of Surgery, Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
Joon Seong ParkDepartment of Surgery, Pancreatobiliary Cancer Clinic, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. jspark330@gmail.com.
Shinae KangDepartment of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. SHINAE95@yuhs.ac.ORCID http://orcid.org/0000-0002-9719-4774

Funding

Yonsei University | Yonsei University College of Medicine (YUCM) 6-2018-0166
6 · The paper itself

Abstract

Diabetes is highly prevalent in individuals with pancreatic ductal adenocarcinoma (PDAC) and even precedes diagnosis of PDAC; however, the mechanisms of pancreatic cancer-associated blood glucose deterioration remain largely unknown. Here, we constructed a prospective cohort of patients undergoing pancreatectomy to investigate the underlying mechanism of PDAC-associated hyperglycemia. A total of 160 patients who underwent pancreatectomy (72 patients with PDAC and 88 patients without PDAC) were enrolled at a tertiary care hospital. Glucometabolic parameters under oral glucose tolerance test were assessed in both pre- and postoperative periods, and patient-derived blood and pancreatic tissue samples were collected. Compared with patients without PDAC, patients with PDAC showed severe hyperglycemia with impaired insulin secretion before surgery. However, despite identical type of pancreatectomy in both groups, hyperglycemia improved more significantly and insulin secretory function declined less after pancreatectomy in patients with PDAC. Plasma Wnt5a and pancreatic islet β-catenin levels were higher in patients with PDAC and correlated with the degree of hyperglycemia and insulin deficiency. Plasma Wnt5a levels also correlated with tumor size and pancreatic islet β-catenin expression in patients with PDAC. In rodent islets, Wnt5a treatment suppressed insulin release, which was recovered by inhibition of β-catenin. Collectively, impaired pancreatic insulin secretion by aberrant Wnt5a/β-catenin activation may underlie the hyperglycemia associated with PDAC. Our finding provides insights into the unique molecular mechanism of pancreatic cancer-associated hyperglycemia, paving the way for the identification of potential biomarker and therapeutic targets for this condition.

Indexed as

beta CateninDiabetes MellitusInsulinInsulin SecretionPancreatic NeoplasmsWnt-5a ProteinAgedAnimalsCarcinoma, Pancreatic DuctalFemaleHumansMaleMiceMiddle AgedPancreatectomySignal Transductionbeta CateninInsulinWnt-5a ProteinWNT5A protein, human

Identifiers

PMID41593307
PMCPMC12868803

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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.