Evidence map›Paper›PMID 42496715›Full record

ArticleCalcified tissue international2026

Gestational Protein Restriction Promotes Osteoporotic Phenotype During Aging.

Bruno Calsa, Saul Lindo-Samanamud, Giovani Vinhato Breanza, Renata Marinho Melo, José Antônio Rocha Gontijo, Milton Santamaria-Jr, Patrícia Aline Boer

Abstract read
In one paragraph

Article in Calcified tissue international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Bruno CalsaFetal Programming and Hydroelectrolyte Metabolism Laboratory, Department of Internal Medicine, School of Medical Sciences, Campinas State University (UNICAMP), Campinas, SP, Brazil.ORCID http://orcid.org/0000-0001-9035-3448
Saul Lindo-SamanamudBrazilian Biosciences National Laboratory (LNBiO), Brazilian Center for Research in Energy and Materials (CNPEM), Campinas, SP, Brazil.
Giovani Vinhato BreanzaDepartment of Social and Paediatric Dentistry, School of Dentistry, Institute of Science and Technology (ICT), São Paulo State University (UNESP), São José dos Campos, São Paulo, Brazil.
Renata Marinho MeloDepartment of Dental Materials and Prosthesis, School of Dentistry, Institute of Science and Technology (ICT), São Paulo State University (UNESP), São José dos Campos, São Paulo, Brazil.
José Antônio Rocha GontijoFetal Programming and Hydroelectrolyte Metabolism Laboratory, Department of Internal Medicine, School of Medical Sciences, Campinas State University (UNICAMP), Campinas, SP, Brazil.
Milton Santamaria-JrDepartment of Social and Paediatric Dentistry, School of Dentistry, Institute of Science and Technology (ICT), São Paulo State University (UNESP), São José dos Campos, São Paulo, Brazil.
Patrícia Aline BoerFetal Programming and Hydroelectrolyte Metabolism Laboratory, Department of Internal Medicine, School of Medical Sciences, Campinas State University (UNICAMP), Campinas, SP, Brazil. boer@unicamp.br.ORCID http://orcid.org/0000-0002-1196-2606

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoporosis results from impaired bone remodeling and deterioration of bone microarchitecture, ultimately increasing fracture risk. Although early-life nutritional stress has been implicated in long-term health outcomes, its impact on skeletal remodeling mechanisms remains unclear. We investigated whether gestational protein restriction induces persistent alterations in the skeletal immune microenvironment that contribute to age-related bone fragility. Pregnant C57BL/6J mice were fed either a normal-protein or low-protein (LP) diet during gestation. Male offspring were evaluated at 12 and 18 months of age. Microcomputed tomography revealed significant reductions in trabecular bone volume fraction, bone mineral density, and trabecular number in 18-month-old LP offspring, along with reduced cortical thickness at both ages. Three-point bending tests demonstrated reduced maximal load in LP-18 M femora, indicating compromised mechanical strength. Ultrastructural analyses revealed increased cortical porosity and disrupted collagen fiber organization in aged LP bone. RNA sequencing identified differentially expressed genes enriched in pathways related to macrophage recruitment, complement signaling, and osteoclast differentiation. RT-qPCR confirmed increased expression of C5ar1, Ccl3, Ccr2, Lilrb4a, and Trem2. Immunohistochemical analysis demonstrated increased CD68

Indexed as

AgingDiet, Protein-RestrictedOsteoporosisPrenatal Exposure Delayed EffectsAnimalsBone and BonesBone DensityBone RemodelingFemaleMaleMiceMice, Inbred C57BLPhenotypePregnancyBone lossDOHaDFemurImmunoporosis

Identifiers

PMID42496715
PMCPMC13400681

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.