Evidence map›Paper›PMID 20720448›Full record

ArticlePancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]2010

Pancreatic function in carboxyl-ester lipase knockout mice.

Mette Vesterhus, Helge Raeder, Amarnath J Kurpad, Dan Kawamori, Anders Molven, Rohit N Kulkarni, C Ronald Kahn, Pål Rasmus Njølstad

Open access · bronzeAbstract read
In one paragraph

Article in Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.], 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  5. Review
  6. Article
  7. The CEL-HYB1 Hybrid Allele Promotes Digestive Enzyme Misfolding and Pancreatitis in Mice.Cellular and molecular gastroenterology and hepatology · 2022
    Article
  8. Monogenic diabetes: a gateway to precision medicine in diabetes.The Journal of clinical investigation · 2021
    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

8 authors at 4 institutions in 2 countries.

Mette VesterhusDepartment of Pediatrics, Haukeland University Hospital, Bergen, Norway.
Helge Raeder
Amarnath J Kurpad
Dan Kawamori
Anders Molven
Rohit N Kulkarni
C Ronald Kahn
Pål Rasmus Njølstad
Joslin Diabetes Center · USUniversity of Bergen · NOHarvard University · USHaukeland University Hospital · NO

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI JEAN E. SCHAFFER · 1986 to 2026
$50.5M
Insulin Receptor Substrates and Insulin ActionR01DK033201 · NIDDK · JOSLIN DIABETES CENTER · PI KAHN, C RONALD · 1986 to 2016
$10.6M
Role of PI 3-Kinase Isoforms in Insulin ActionR01DK055545 · NIDDK · JOSLIN DIABETES CENTER · PI KAHN, C RONALD · 1999 to 2020
$8.3M
Role of IGF-1 and Insulin Receptors Beta-Cell SurvivalR01DK067536 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 2004 to 2026
$8.0M
NIDDK NIH HHS 5P30DK36836NIDDK NIH HHS DK33201NIDDK NIH HHS DK34834NIDDK NIH HHS DK55545NIDDK NIH HHS P30 DK036836NIDDK NIH HHS R01 DK033201NIDDK NIH HHS R01 DK055545NIDDK NIH HHS R01 DK067536NIDDK NIH HHS R01 DK 67536
6 · The paper itself

Abstract

BACKGROUND/

aimsCEL-MODY is a monogenic form of diabetes and exocrine pancreatic insufficiency due to mutations in the carboxyl-ester lipase (CEL) gene. We aimed to investigate endocrine and exocrine pancreatic function in CEL knockout mice (CELKO).

methodsA knockout mouse model with global targeted deletion of CEL was investigated physiologically and histopathologically, and compared to littermate control CEL+/+ mice at 7 and 12 months on normal chow and high-fat diets (HFD), i.e. 42 and 60% fat by calories.

resultsCELKO+/+ and -/- mice showed normal growth and development and normal glucose metabolism on a chow diet. Female CEL-/- mice on 60% HFD, on the other hand, had increased random blood glucose compared to littermate controls (p = 0.02), and this was accompanied by a reduction in glucose tolerance that did not reach statistical significance. In these mice there was also islet hyperplasia, however, α- and β-islet cells appeared morphologically normal and pancreatic exocrine function was also normal.

conclusionAlthough we observed mild glucose intolerance in female mice with whole-body knockout of CEL, the full phenotype of human CEL-MODY was not reproduced, suggesting that the pathogenic mechanisms involved are more complex than a simple loss of CEL function. and IAP.

Indexed as

AnimalsBlood GlucoseDisease Models, AnimalFemaleGlucagon-Secreting CellsGlucose Tolerance TestInsulin-Secreting CellsIntestinal AbsorptionIslets of LangerhansLipaseLongevityMaleMiceMice, Inbred C57BLMice, KnockoutPancreas, ExocrineBlood GlucoseLipase

Identifiers

PMID20720448
PMCPMC2968766
OpenAlexW2004247073

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.