Evidence map›Paper›PMID 26167074›Full record

ArticleWorld journal of gastroenterology2015

Effect of endogenous cholecystokinin on the course of acute pancreatitis in rats.

Dongmei Jia, Mitsuyoshi Yamamoto, Makoto Otsuki

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

Article in World journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 34% 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

3 citing papers in PubMed, 9 citations in OpenAlex.

  1. The role of autophagy in pancreatic diseases.Frontiers in pharmacology · 2024
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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

3 authors at 1 institution in 2 countries.

Dongmei JiaDongmei Jia, Department of Gastroenterology and Metabolism, University of Occupational and Environmental Health, Japan, School of Medicine, Kitakyushu 807-8555, Japan.
Mitsuyoshi YamamotoDongmei Jia, Department of Gastroenterology and Metabolism, University of Occupational and Environmental Health, Japan, School of Medicine, Kitakyushu 807-8555, Japan.
Makoto OtsukiDongmei Jia, Department of Gastroenterology and Metabolism, University of Occupational and Environmental Health, Japan, School of Medicine, Kitakyushu 807-8555, Japan.
The University of Kitakyushu · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo examine the effects of pancreatic rest, stimulation and rest/stimulation on the natural course of recovery after acute pancreatitis.

methodsAcute hemorrhagic pancreatitis (AP) was induced in male rats by intraductal infusion of 40 μL/100 g body weight of 3% sodium taurocholate. All rats took food ad libitum. At 24 h after induction of AP, rats were divided into four groups: control (AP-C), pancreas rest (AP-R), stimulation (AP-S), and rest/stimulation (AP-R/S). Rats in the AP-C, AP-R and AP-S groups received oral administration of 2 mL/kg body weight saline, cholecystokinin (CCK)-1 receptor antagonist, and endogenous CCK release stimulant, respectively, twice daily for 10 d, while those in the AP-R/S group received twice daily CCK-1 receptor antagonist for the first 5 d followed by twice daily CCK release stimulant for 5 d. Rats without any treatment were used as control group (Control). Biochemical and histological changes in the pancreas, and secretory function were evaluated on day 12 at 24 h after the last treatment.

resultsFeeding ad libitum (AP-C) delayed biochemical, histological and functional recovery from AP. In AP-C rats, bombesin-stimulated pancreatic secretory function and HOMA-β-cell score were significantly lower than those in other groups of rats. In AP-R rats, protein per DNA ratio and pancreatic exocrine secretory function were significantly low compared with those in Control rats. In AP-S and AP-R/S rats, the above parameters recovered to the Control levels. Bombesin-stimulated pancreatic exocrine response in AP-R/S rats was higher than in AP-S rats and almost returned to control levels. In the pancreas of AP-C rats, destruction of pancreatic acini, marked infiltration of inflammatory cells, and strong expression of α-smooth muscle actin, tumor necrosis factor-α and interleukin-1β were seen. Pancreatic rest reversed these histological alterations, but not atrophy of pancreatic acini and mild infiltration of inflammatory cells. In AP-S and AP-R/S rats, the pancreas showed almost normal architecture.

conclusionThe favorable treatment strategy for AP is to keep the pancreas at rest during an early stage followed by pancreatic stimulation by promoting endogenous CCK release.

Indexed as

Administration, OralAnimalsBiomarkersBombesinCell ProliferationCholecystokininDisease Models, AnimalDNA ReplicationEstersGabexateGuanidinesHormone AntagonistsInsulin ResistanceMalePancreasPancreatic Function TestsBiomarkersBombesincamostatCholecystokininEstersGabexateGuanidinesHormone AntagonistsloxiglumideProglumideReceptor, Cholecystokinin ATaurocholic AcidAcute pancreatitisCholecystokininPancreatic functionPancreatic restPancreatic stimulation

Identifiers

PMID26167074
PMCPMC4491961
OpenAlexW2409669158

What OpenQuestion holds

Textmetadata
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.