Evidence map›Paper›PMID 25918019›Full record

ArticleBiochemical and biophysical research communications2015

Overexpression of Pref-1 in pancreatic islet β-cells in mice causes hyperinsulinemia with increased islet mass and insulin secretion.

Yuhui Wang, Kichoon Lee, Yang Soo Moon, Maryam Ahmadian, Kee-Hong Kim, Karim Roder, Chulho Kang, Hei Sook Sul

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  6. Article
  7. 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.

Yuhui WangDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, CA 94720, USA.
Kichoon LeeDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, CA 94720, USA.
Yang Soo MoonDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, CA 94720, USA.
Maryam AhmadianDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, CA 94720, USA.
Kee-Hong KimDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, CA 94720, USA.
Karim RoderDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, CA 94720, USA.
Chulho KangDepartment of Molecular Cell Biology, University of California, Berkeley, CA 94720, USA.
Hei Sook SulDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, CA 94720, USA. Electronic address: hsul@berkeley.edu.
University of California, Berkeley · US

Funding

REGULATION OF PREF-1 GENE IN ADIPOCYTE DIFFERENTIATIONR01DK050828 · NIDDK · UNIVERSITY OF CALIFORNIA BERKELEY · PI SUL, HEI SOOK · 1995 to 2013
$3.5M
Pre-doctoral Training in Molecular and Biochemical NutritionT32DK061918 · NIDDK · UNIVERSITY OF CALIFORNIA BERKELEY · PI NAPOLI, JOSEPH L · 2002 to 2016
$2.6M
NIDDK NIH HHS DK 50828NIDDK NIH HHS R01 DK050828NIDDK NIH HHS T32 DK061918
6 · The paper itself

Abstract

Preadipocyte factor-1 (Pref-1) is made as a transmembrane protein containing EGF-repeats at the extracellular domain that can be cleaved to generate a biologically active soluble form. Pref-1 is found in islet β-cells and its level has been reported to increase in neonatal rat islets upon growth hormone treatment. We found here that Pref-1 can promote growth of pancreatic tumor derived AR42J cells. To examine Pref-1 function in pancreatic islets in vivo, we generated transgenic mouse lines overexpressing the Pref-1/hFc in islet β-cells using rat insulin II promoter (RIP). These transgenic mice exhibit an increase in islet mass with higher proportion of larger islets in pancreas compared to wild-type littermates. This is in contrast to pancreas from Pref-1 null mice that show higher proportion of smaller islets. Insulin expression and insulin secretion from pancreatic islets from RIP-Pref-1/hFc transgenic mice are increased also. Thus, RIP-Pref-1/hFc transgenic mice show normal glucose levels but with higher plasma insulin levels in both fasting and fed conditions. These mice show improved glucose tolerance. Taken together, we conclude Pref-1 as a positive regulator of islet β-cells and insulin production.

Indexed as

Cell ProliferationAnimalsCalcium-Binding ProteinsFemaleHyperinsulinismInsulinInsulin ResistanceInsulin-Secreting CellsInsulin SecretionIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMice, TransgenicUp-RegulationCalcium-Binding ProteinsDlk1 protein, mouseInsulinIntercellular Signaling Peptides and ProteinsDiabetesHyperinsulinemiaInsulin secretionIslet β-cellsPref-1/Dlk1Transgenic mice

Identifiers

PMID25918019
PMCPMC4439292
OpenAlexW1972090266

What OpenQuestion holds

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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.