Evidence map›Paper›PMID 30269370›Full record

ArticleJournal of cellular biochemistry2019

Novel leptin receptor signaling mutants identify location and sex-dependent modulation of bone density, adiposity, and growth.

Ian C McCabe, Alyssa Fedorko, Martin G Myers, Gina Leinninger, Erica Scheller, Laura R McCabe

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Osteoporosis and Leptin: A Systematic Review.Iranian journal of public health · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. ΔFosB Requires Galanin, but not Leptin, to Increase Bone Mass via the Hypothalamus, but both are needed to increase Energy expenditure.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019
    Article
  11. 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

6 authors at 3 institutions in 1 country.

Ian C McCabeDepartment of Physiology, Michigan State University, East Lansing, Michigan.
Alyssa FedorkoDepartment of Physiology, Michigan State University, East Lansing, Michigan.
Martin G MyersDepartment of Molecular and Integrative Physiology, Division of Metabolism, Endocrinology and Diabetes, University of Michigan, Ann Arbor, Michigan.
Gina LeinningerDepartment of Physiology, Michigan State University, East Lansing, Michigan.
Erica SchellerDepartment of Medicine, Division of Bone and Mineral Diseases, Washington University, Saint Louis, Missouri.
Laura R McCabeDepartment of Physiology, Michigan State University, East Lansing, Michigan.ORCID 0000-0001-5407-162X
Michigan State University · USUniversity of Michigan · USWashington University in St. Louis · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
MOLECULAR DETERMINANTS OF LEPTIN RECEPTOR/JAK2 SIGNALINGR01DK056731 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 1999 to 2025
$6.0M
Mechanistic basis of probiotic prevention of osteoporosisR01AT007695 · NCCIH · MICHIGAN STATE UNIVERSITY · PI BRITTON, ROBERT A, MCCABE, LAURA R · 2013 to 2017
$2.2M
The Role of the Gut and Bone Microenvironment in T1D Bone LossR01DK101050 · NIDDK · MICHIGAN STATE UNIVERSITY · PI MCCABE, LAURA R, PARAMESWARAN, NARAYANAN · 2014 to 2016
$1.1M
Neural regulation of skeletal biology and periodontal disease progression in typeR00DE024178 · NIDCR · WASHINGTON UNIVERSITY · PI SCHELLER, ERICA LYNN · 2016 to 2018
$735k
NCCIH NIH HHS R01 AT007695NIDCR NIH HHS R00 DE024178NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK056731NIDDK NIH HHS R01 DK101050
6 · The paper itself

Abstract

Leptin, a hormone primarily produced by adipocytes, contributes to the regulation of bone health by modulating bone density, growth and adiposity. Upon leptin binding, multiple sites of the long form of the leptin receptor (LepRb) are phosphorylated to trigger activation of downstream signaling pathways. To address the role of LepRb-signaling pathways in bone health, we compared the effects of three LepRb mutations on bone density, adiposity, and growth in male and female mice. The ∆65 mutation, which lacks the known tyrosine phosphorylation sites, caused obesity and the most dramatic bone phenotype marked by excessive bone adiposity, osteoporosis, and decreased growth, consistent with the phenotype of db/db and ob/ob mice that fully lack leptin receptor signaling. Mutation of LepRb Tyr

Indexed as

Sex CharacteristicsAdipocytes, WhiteAdiposityAnimalsBone DensityCancellous BoneFemaleFemurLeptinMaleMiceMice, Mutant StrainsMutationProtein Tyrosine Phosphatase, Non-Receptor Type 11Receptors, LeptinSignal TransductionLeptinProtein Tyrosine Phosphatase, Non-Receptor Type 11Receptors, LeptinSocs3 protein, mouseSuppressor of Cytokine Signaling 3 Proteinadipocytesbone densitybone volumefemaleleptin receptormalemarrow adiposityobesityosteoporosis

Identifiers

PMID30269370
PMCPMC6336499
OpenAlexW2893538102

What OpenQuestion holds

Textmetadata
LicenceTDM
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.