Evidence map›Paper›PMID 22515107›Full record

ReviewNagoya journal of medical science2012

Physiology and pathophysiology of bicarbonate secretion by pancreatic duct epithelium.

Hiroshi Ishiguro, Akiko Yamamoto, Miyuki Nakakuki, Lanjuan Yi, Mariko Ishiguro, Makoto Yamaguchi, Shiho Kondo, Yuka Mochimaru

Open access · greenAbstract readReview
In one paragraph

Review in Nagoya journal of medical science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 63 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. T1 Mapping of the Abdomen, From theAJR. American journal of roentgenology · 2025
    Review
  7. The function of chloride channels in digestive system disease (Review).International journal of molecular medicine · 2025
    Review
  8. Article
  9. Article
  10. Advances in MRI of Chronic Pancreatitis.Advances in clinical radiology · 2024
    Article
  11. Bicarbonate secretion and acid/base sensing by the intestine.Pflugers Archiv : European journal of physiology · 2024
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Gelsolin inhibits autophagy by regulating actin depolymerization in pancreatic ductal epithelial cells in acute pancreatitis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023
    Article
  20. 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

8 authors at 1 institution in 1 country.

Hiroshi IshiguroLaboratory of Human Nutrition, Nagoya University Graduate School of Medicine, Nagoya, Japan. ishiguro@htc.nagoya-u.ac.jp
Akiko Yamamoto
Miyuki Nakakuki
Lanjuan Yi
Mariko Ishiguro
Makoto Yamaguchi
Shiho Kondo
Yuka Mochimaru
Nagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HCO3- -rich fluid in the pancreatic juice (2-3 L/day) is secreted by epithelial cells lining the pancreatic duct tree, while digestive enzymes are secreted by acinar cells with a small amount of Cl- -rich fluid. Ductal HCO3- secretion is not only regulated by gastrointestinal hormones and cholinergic nerves but is also influenced by luminal factors: intraductal pressure, Ca2+ concentration, pathological activation of protease and bile reflux. The maximum HCO3- concentration of the juice under secretin stimulation reaches 140-150 mM. Thus pancreatic duct cells secrete HCO3- against a approximately 7-fold concentration gradient. HCO3- secretion critically depends on the activity of CFTR, a cAMP-dependent anion channel localized in the apical membrane of various epithelia. In the proximal part of pancreatic ducts close to acinar cells HCO3 secretion across the apical membrane is largely mediated by SLC26A6 CI- -HCO3- exchanger. In distal ducts where the luminal HCO3- concentration is already high, most of the HCO3- secretion is mediated by HCO3- conductance of CFTR. CFTR is the causative gene for cystic fibrosis. Loss of function due to severe mutations in both alleles causes typical cystic fibrosis characterized by dehydrated, thick, and viscous luminal fluid/mucus in the respiratory and gastrointestinal tract, pancreatic duct, and vas deferens. A compound heterozygote of mutations/polymorphisms (causing a mild dysfunction of CFTR) involves a risk of developing CFTR-related diseases such as chronic pancreatitis. In cystic fibrosis and certain cases of chronic pancreatitis, the pancreatic duct epithelium secretes a small amount of fluid with neutral-acidic pH, which causes an obstruction of the duct lumen by a protein plug or viscous mucus.

Indexed as

AnimalsBicarbonatesBiological Transport, ActiveCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorEpithelial CellsEthanolGlucoseHumansPancreatic DiseasesPancreatic DuctsPancreatic JuiceBicarbonatesCystic Fibrosis Transmembrane Conductance RegulatorEthanolGlucose

Identifiers

PMID22515107
PMCPMC4831246
OpenAlexW1507988153

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.