Evidence map›Paper›PMID 28874358›Full record

Trial reportAmerican journal of physiology. Endocrinology and metabolism2017

Soluble interleukin-13rα1: a circulating regulator of glucose.

Inbal Rachmin, Caitlin C O'Meara, Elisabeth M Ricci-Blair, Yilin Feng, Emily M Christensen, Jeanne F Duffy, Kirsi M Zitting, Charles A Czeisler, James R Pancoast, Christopher P Cannon and 3 more

Open access · bronzeAbstract readMulticenter StudyRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in American journal of physiology. Endocrinology and metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Review
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

13 authors at 3 institutions in 1 country.

Inbal RachminDepartment of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts.
Caitlin C O'MearaDepartment of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts.
Elisabeth M Ricci-BlairDepartment of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts.
Yilin FengDepartment of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts.
Emily M ChristensenDepartment of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts.
Jeanne F DuffyDivision of Sleep and Circadian Disorders, Departments of Medicine and Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; and.
Kirsi M ZittingDivision of Sleep and Circadian Disorders, Departments of Medicine and Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; and.
Charles A CzeislerDivision of Sleep and Circadian Disorders, Departments of Medicine and Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; and.
James R PancoastDepartment of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts.
Christopher P CannonDivision of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Michelle L O'DonoghueDivision of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
David A MorrowDivision of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Richard T LeeDepartment of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts; richard_lee@harvard.edu.
Harvard University · USBrigham and Women's Hospital · USHarvard Stem Cell Institute · US

Funding

Harvard Clinical and Translational Science CenterUL1TR001102 · NCATS · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2013 to 2017
$106.2M
Zoledronic Acid in Treatment of Osteoporosis in PostmenoM01RR002635 · NCRR · BRIGHAM AND WOMEN'S HOSPITAL · PI WILLIAMS, GORDON H · 1985 to 2008
$48.4M
A New Pathway for Reversing Cardiac AgingR01AG047131 · NIA · HARVARD UNIVERSITY · PI LEE, RICHARD T · 2015 to 2019
$1.7M
Reprogramming Non-myocytes to Cardiomyocytes in vivoR01HL119230 · NHLBI · HARVARD UNIVERSITY · PI LEE, RICHARD T · 2016 to 2019
$1.7M
Biasing Myocardial Neuregulin Signaling with Engineered LigandsR01HL117986 · NHLBI · HARVARD UNIVERSITY · PI LEE, RICHARD T · 2013 to 2016
$1.6M
Circadian & Genetic Evaluation of Extreme Sleep TimingR01HL080978 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI DUFFY, JEANNE F · 2006 to 2009
$1.2M
NCATS NIH HHS UL1 TR001102NCRR NIH HHS M01 RR002635NHLBI NIH HHS R01 HL080978NHLBI NIH HHS R01 HL117986NHLBI NIH HHS R01 HL119230NIA NIH HHS R01 AG047131
6 · The paper itself

Abstract

Soluble IL-13 receptor-α1, or sIL13rα1, is a soluble protein that binds to interleukin-13 (IL-13) that has been previously described in mice. The function of sIL13rα1 remains unclear, but it has been hypothesized to act as a decoy receptor for IL-13. Recent studies have identified a role for IL-13 in glucose metabolism, suggesting that a decoy receptor for IL-13 might increase circulating glucose levels. Here, we report that delivery of sIL13rα1 to mice by either gene transfer or recombinant protein decreases blood glucose levels. Surprisingly, the glucose-lowering effect of sIL13rα1 was preserved in mice lacking IL-13, demonstrating that IL-13 was not required for the effect. In contrast, deletion of IL-4 in mice eliminated the hypoglycemic effect of sIL13rα1. In humans, endogenous blood levels of IL13rα1 varied substantially, although there were no differences between diabetic and nondiabetic patients. There was no circadian variation of sIL13rα1 in normal human volunteers. Delivery of sIL13rα1 fused to a fragment crystallizable (Fc) domain provided sustained glucose lowering in mice on a high-fat diet, suggesting a potential therapeutic strategy. These data reveal sIL13rα1 as a circulating human protein with an unexpected role in glucose metabolism.

Indexed as

AdolescentAdultAgedAnimalsCarbohydrate MetabolismFemaleGlucoseHumansHypoglycemic AgentsInterleukin-13 Receptor alpha1 SubunitInterleukin-4MaleMiceMice, Inbred C57BLMice, KnockoutMiddle AgedGlucoseHypoglycemic AgentsIL13RA1 protein, humanInterleukin-13 Receptor alpha1 SubunitInterleukin-4Recombinant Proteinsfasting glucoseinterleukinssoluble receptors

Identifiers

PMID28874358
PMCPMC5814599
OpenAlexW2750717178

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.