Evidence map›Paper›PMID 33250773›Full record

ReviewFrontiers in physiology2020

Pathological Mechanisms in Diabetes of the Exocrine Pancreas: What's Known and What's to Know.

Qiong Wei, Liang Qi, Hao Lin, Dechen Liu, Xiangyun Zhu, Yu Dai, Richard T Waldron, Aurelia Lugea, Mark O Goodarzi, Stephen J Pandol and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 40 citations in OpenAlex.

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  16. A Review on the Antidiabetic Properties ofFrontiers in pharmacology · 2022
    Review
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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

11 authors at 3 institutions in 2 countries.

Qiong WeiDepartment of Endocrinology, ZhongDa Hospital, School of Medicine, Southeast University, Nanjing, China.
Liang QiDepartment of Endocrinology, ZhongDa Hospital, School of Medicine, Southeast University, Nanjing, China.
Hao LinInstitute of Pancreas, Southeast University, Nanjing, China.
Dechen LiuInstitute of Pancreas, Southeast University, Nanjing, China.
Xiangyun ZhuDepartment of Endocrinology, ZhongDa Hospital, School of Medicine, Southeast University, Nanjing, China.
Yu DaiNanjing Foreign Language School, Nanjing, China.
Richard T WaldronDivision of Gastroenterology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Aurelia LugeaDivision of Gastroenterology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Mark O GoodarziDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Stephen J PandolDivision of Gastroenterology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Ling LiDepartment of Endocrinology, ZhongDa Hospital, School of Medicine, Southeast University, Nanjing, China.
Zhongda Hospital Southeast University · CNCedars-Sinai Medical Center · USNanjing Foreign Language School · CN

Funding

Project 3: Role of the pancreatic fibroinflammatory microenvironment in obesity-promoted pancreatic cancerP01CA236585 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI EIBL, GUIDO ERWIN MICHAEL · 2020 to 2024
$5.6M
NCI NIH HHS P01 CA236585
6 · The paper itself

Abstract

The clinical significance of diabetes arising in the setting of pancreatic disease (also known as diabetes of the exocrine pancreas, DEP) has drawn more attention in recent years. However, significant improvements still need to be made in the recognition, diagnosis and treatment of the disorder, and in the knowledge of the pathological mechanisms. The clinical course of DEP is different from type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). DEP develops in patients with previous existing exocrine pancreatic disorders which damage both exocrine and endocrine parts of pancreas, and lead to pancreas exocrine insufficiency (PEI) and malnutrition. Therefore, damage in various exocrine and endocrine cell types participating in glucose metabolism regulation likely contribute to the development of DEP. Due to the limited amount of clinical and experimental studies, the pathological mechanism of DEP is poorly defined. In fact, it still not entirely clear whether DEP represents a distinct pathologic entity or is a form of T2DM arising when β cell failure is accelerated by pancreatic disease. In this review, we include findings from related studies in T1DM and T2DM to highlight potential pathological mechanisms involved in initiation and progression of DEP, and to provide directions for future research studies.

Indexed as

chronic pancreatitisdiabetesendocrineexocrine pancreaspathological mechanisms

Identifiers

PMID33250773
PMCPMC7673428
OpenAlexW3097852687

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.