Evidence map›Paper›PMID 24955854›Full record

ArticleBiochemical and biophysical research communications2014

Palmitate attenuates osteoblast differentiation of fetal rat calvarial cells.

Lee-Chuan C Yeh, Jeffery J Ford, John C Lee, Martin L Adamo

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

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  10. The investigation of energy metabolism in osteoblasts and osteoclasts.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2021
    Article
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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

4 authors.

Lee-Chuan C YehDepartment of Biochemistry, The University of Texas Health Science Center at San Antonio, TX, United States.
Jeffery J FordDepartment of Biochemistry, The University of Texas Health Science Center at San Antonio, TX, United States.
John C LeeDepartment of Biochemistry, The University of Texas Health Science Center at San Antonio, TX, United States; The Sam and Ann Barshop Institute for Longevity and Aging Studies, The University of Texas Health Science Center at San Antonio, TX, United States.
Martin L AdamoDepartment of Biochemistry, The University of Texas Health Science Center at San Antonio, TX, United States; The Sam and Ann Barshop Institute for Longevity and Aging Studies, The University of Texas Health Science Center at San Antonio, TX, United States. Electronic address: adamo@biochem.uthscsa.edu.

Funding

mTOR Signaling and Bone Formation in Aging SkeletonR21AG040612 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ADAMO, MARTIN L, LEE, JOHN C · 2012 to 2013
$398k
NIA NIH HHS R21 AG040612NIA NIH HHS R21AG040612
6 · The paper itself

Abstract

Aging is associated with the accumulation of ectopic lipid resulting in the inhibition of normal organ function, a phenomenon known as lipotoxicity. Within the bone marrow microenvironment, elevation in fatty acid levels may produce an increase in osteoclast activity and a decrease in osteoblast number and function, thus contributing to age-related osteoporosis. However, little is known about lipotoxic mechanisms in intramembraneous bone. Previously we reported that the long chain saturated fatty acid palmitate inhibited the expression of the osteogenic markers RUNX2 and osteocalcin in fetal rat calvarial cell (FRC) cultures. Moreover, the acetyl CoA carboxylase inhibitor TOFA blocked the inhibitory effect of palmitate on expression of these two markers. In the current study we have extended these observations to show that palmitate inhibits spontaneous mineralized bone formation in FRC cultures in association with reduced mRNA expression of RUNX2, alkaline phosphatase, osteocalcin, and bone sialoprotein and reduced alkaline phosphatase activity. The effects of palmitate on osteogenic marker expression were inhibited by TOFA. Palmitate also inhibited the mRNA expression of fatty acid synthase and PPARγ in FRC cultures, and as with osteogenic markers, this effect was inhibited by TOFA. Palmitate had no effect on FRC cell proliferation or apoptosis, but inhibited BMP-7-induced alkaline phosphatase activity. We conclude that palmitate accumulation may lead to lipotoxic effects on osteoblast differentiation and mineralization and that increases in fatty acid oxidation may help to prevent these lipotoxic effects.

Indexed as

AnimalsCell DifferentiationCells, CulturedDose-Response Relationship, DrugEmbryonic Stem CellsOsteoblastsOsteogenesisPalmitatesRatsSkullPalmitatesFetal rat calvarial cell cultureLipotoxicityOsteoblast differentiationPalmitate

Identifiers

PMID24955854
PMCPMC4118421

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Registered trials

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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.