Evidence map›Paper›PMID 38360197›Full record

ArticleBone2024

Abaloparatide is more potent than teriparatide in restoring bone mass and strength in type 1 diabetic male mice.

Silvia Marino, Serra Ucer Ozgurel, Kevin McAndrews, Meloney Cregor, Alma Villaseñor, Maricuz Mamani-Huanca, Coral Barbas, Arancha Gortazar, Amy Y Sato, Teresita Bellido

Abstract read
In one paragraph

Article in Bone, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

3 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

10 authors at 4 institutions in 2 countries.

Silvia MarinoDepartment of Physiology and Cell Biology, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Central Arkansas Veterans Healthcare System, John L. McClellan Little Rock, AR, USA. Electronic address: SMarino@uams.edu.
Serra Ucer OzgurelIndiana University School of Medicine, Indianapolis, IN, USA; Roudebush Veterans Administration Medical Center, Indianapolis, IN, USA. Electronic address: sucerozgurel@austin.utexas.edu.
Kevin McAndrewsIndiana University School of Medicine, Indianapolis, IN, USA; Roudebush Veterans Administration Medical Center, Indianapolis, IN, USA. Electronic address: kmcandre@iupui.edu.
Meloney CregorDepartment of Physiology and Cell Biology, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Central Arkansas Veterans Healthcare System, John L. McClellan Little Rock, AR, USA; Indiana University School of Medicine, Indianapolis, IN, USA; Roudebush Veterans Administration Medical Center, Indianapolis, IN, USA. Electronic address: mcregor@iupui.edu.
Alma VillaseñorCentre for Metabolomics and Bioanalysis (CEMBIO), Faculty of Pharmacy, Universidad San Pablo-CEU, CEU Universities, Campus Monteprincipe, 28925 Alcorcón, Madrid, Spain. Electronic address: alma.villasenor@ceu.es.
Maricuz Mamani-HuancaCentre for Metabolomics and Bioanalysis (CEMBIO), Faculty of Pharmacy, Universidad San Pablo-CEU, CEU Universities, Campus Monteprincipe, 28925 Alcorcón, Madrid, Spain. Electronic address: maricuz.mamanihuanca@ceu.es.
Coral BarbasCentre for Metabolomics and Bioanalysis (CEMBIO), Faculty of Pharmacy, Universidad San Pablo-CEU, CEU Universities, Campus Monteprincipe, 28925 Alcorcón, Madrid, Spain. Electronic address: cbarbas@ceu.es.
Arancha GortazarBone Physiopathology laboratory, Applied Molecular Medicine Institute (IMMA), Universidad San Pablo-CEU, CEU Universities, Campus Monteprincipe, 28925 Alcorcón, Madrid, Spain. Electronic address: argortazar@ceu.es.
Amy Y SatoDepartment of Physiology and Cell Biology, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Central Arkansas Veterans Healthcare System, John L. McClellan Little Rock, AR, USA; Indiana University School of Medicine, Indianapolis, IN, USA; Roudebush Veterans Administration Medical Center, Indianapolis, IN, USA. Electronic address: AYSato@uams.edu.
Teresita BellidoDepartment of Physiology and Cell Biology, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Central Arkansas Veterans Healthcare System, John L. McClellan Little Rock, AR, USA; Indiana University School of Medicine, Indianapolis, IN, USA; Roudebush Veterans Administration Medical Center, Indianapolis, IN, USA. Electronic address: tmbellido@uams.edu.
Universidad San Pablo CEU · ESCentral Arkansas Veterans Healthcare System · USIndiana University – Purdue University Indianapolis · USRichard L. Roudebush VA Medical Center · US

Funding

Comprehensive Training Program in Musculoskeletal ResearchT32AR065971 · NIAMS · INDIANA UNIVERSITY INDIANAPOLIS · PI ALEXANDER G ROBLING · 2015 to 2026
$4.4M
Glucocorticoid-induced Atrophy in Bone and MuscleR01AR059357 · NIAMS · UNIV OF ARKANSAS FOR MED SCIS · PI BELLIDO, TERESITA M. · 2011 to 2022
$3.4M
BLRD VA I01 BX002104BLRD VA IK6 BX004596NIAMS NIH HHS R01 AR059357NIAMS NIH HHS T32 AR065971
6 · The paper itself

Abstract

This study investigated the efficacy of the two FDA-approved bone anabolic ligands of the parathyroid hormone receptor 1 (PTH1R), teriparatide or human parathyroid hormone 1-34 (PTH) and abaloparatide (ABL), to restoring skeletal health using a preclinical murine model of streptozotocin-induced T1-DM. Intermittent daily subcutaneous injections of equal molar doses (12 pmoles/g/day) of PTH (50 ng/g/day), ABL (47.5 ng/g/day), or vehicle, were administered for 28 days to 5-month-old C57Bl/6 J male mice with established T1-DM or control (C) mice. ABL was superior to PTH in increasing or restoring bone mass in control or T1-MD mice, respectively, which was associated with superior stimulation of trabecular and periosteal bone formation, upregulation of osteoclastic/osteoblastic gene expression, and increased circulating bone remodeling markers. Only ABL corrected the reduction in ultimate load, which is a measure of bone strength, induced by T1-DM, and it also increased energy to ultimate load. In addition, bones from T1-DM mice treated with PTH or ABL exhibited increased ultimate stress, a material index, compared to T1-DM mice administered with vehicle. And both PTH and ABL prevented the increased expression of the Wnt antagonist Sost/sclerostin displayed by T1-DM mice. Further, PTH and ABL increased to a similar extent the circulating bone resorption marker CTX and the bone formation marker P1NP in T1-DM after 2 weeks of treatment; however, only ABL sustained these increases after 4 weeks of treatment. We conclude that at equal molar doses, ABL is more effective than PTH in increasing bone mass and restoring the cortical and trabecular bone lost with T1-DM, due to higher and longer-lasting increases in bone remodeling.

Indexed as

Diabetes Mellitus, Type 1TeriparatideAnimalsBone DensityHumansInfant, NewbornMaleMiceParathyroid HormoneParathyroid Hormone-Related ProteinabaloparatideParathyroid HormoneParathyroid Hormone-Related ProteinTeriparatideAbaloparatideBoneDiabetesPTH

Identifiers

PMID38360197
PMCPMC13147481
OpenAlexW4391787621

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.