Evidence map›Paper›PMID 11121384›Full record

ArticleAmerican journal of physiology. Cell physiology2001

Defective dietary fat processing in transgenic mice lacking aquaporin-1 water channels.

T Ma, S Jayaraman, K S Wang, Y Song, B Yang, J Li, J A Bastidas, A S Verkman

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2001. 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 7% 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, 118 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Aquaporins Involvement in Pancreas Physiology and in Pancreatic Diseases.International journal of molecular sciences · 2019
    Review
  11. Review
  12. Nuclear Receptor Regulation of Aquaglyceroporins in Metabolic Organs.International journal of molecular sciences · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. 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 2 institutions in 1 country.

T MaDepartment of Medicine, Cardiovascular Research Institute, University of California, San Francisco 94143-0521, California, USA.
S Jayaraman
K S Wang
Y Song
B Yang
J Li
J A Bastidas
A S Verkman
University of California, San Francisco · USStanford University · US

Funding

MECHANISMS OF WATER TRANSPORT IN RENAL EPITHELIAR37DK035124 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VERKMAN, ALAN S · 1999 to 2008
$4.2M
SEROUS CELL MALFUNCTION AND CYSTIC FIBROSIS LUNG DISEASEP50HL060288 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI WINE, JEFFREY J · 1998 to 2002
$2.8M
PHYSIOLOGY AND MOLECULAR BIOLOGY OF LUNG WATER TRANSPORTR01HL059198 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VERKMAN, ALAN S · 1998 to 2007
$2.2M
WATER AND NON-ELECTROLYTE TRANSPORT IN RENAL VESICLESR01DK035124 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI VERKMAN, ALAN S · 1986 to 2014
$1.4M
AQUAPORINS AND INTESTINAL WATER TRANSPORTF32DK009526 · NIDDK · STANFORD UNIVERSITY · PI WANG, KASPER S · 1997 to 1998
–
NHLBI NIH HHS HL-59198NHLBI NIH HHS HL-60288NHLBI NIH HHS R01 HL059198NIDDK NIH HHS DK-35124NIDDK NIH HHS F32 DK009526NIDDK NIH HHS R01 DK035124NIDDK NIH HHS R37 DK035124
6 · The paper itself

Abstract

Immunocytochemistry showed expression of aquaporin-1 (AQP1) water channels at sites involved in dietary fat processing, including intrahepatic cholangiocytes, gallbladder, pancreatic microvascular endothelium, and intestinal lacteals. To determine whether AQP1 has a role in dietary fat digestion and/or absorption, mice were placed on a diet that contained 50% fat. Whereas wild-type mice (3-3.5 wk of age, 10-12 g) gained 49 +/- 5% (SE, n = 50) body weight in 8 days, and heterozygous mice gained 46 +/- 4%, AQP1 null mice gained only 4 +/- 3%; weights became similar after return to a 6% fat diet after 6 days. The null mice on a high-fat diet acquired an oily appearance, developed steatorrhea with increased stool triglyceride content, and manifested serum hypotriglyceridemia. Supplementation of the high-fat diet with pancreatic enzymes partially corrected the decreased weight gain in null mice. Absorption of [(14)C]oleic acid from small intestine was not affected by AQP1 deletion, as determined by blood radioactivity after duodenal infusion. Lipase activity in feces and small intestine was remarkably greater in AQP1 null than wild-type mice on low- and high-fat diets. Fluid collections done in older mice (that are less sensitive to a high-fat diet) by ductal cannulation showed threefold increased pancreatic fluid flow in response to secretin/cholecystokinin, but volumes, pH, and amylase activities were affected little by AQP1 deletion, nor were bile flow rates and bile salt concentrations. Together, these results establish a dietary fat misprocessing defect in AQP1 null mice.

Indexed as

Age FactorsAnimalsAquaporin 1AquaporinsBody WeightCeliac DiseaseDietary FatsDigestive SystemDigestive System DiseasesEatingFatty AcidsFood, FormulatedGallbladderIntestine, SmallLipaseLiverAqp1 protein, mouseAquaporin 1AquaporinsDietary FatsFatty AcidsLipasePancrelipase

Identifiers

PMID11121384
PMCPMC3491804
OpenAlexW2138651864

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.