Evidence map›Paper›PMID 24928196›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014

Overweight and CpG methylation of the Pomc promoter in offspring of high-fat-diet-fed dams are not "reprogrammed" by regular chow diet in rats.

Asaf Marco, Tatiana Kisliouk, Tzlil Tabachnik, Noam Meiri, Aron Weller

Open access · greenAbstract readComparative Study
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
19.2field-weighted citation impact, top 1% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
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  12. DNA Methylation in the Hypothalamic Feeding Center and Obesity.Journal of obesity & metabolic syndrome · 2023
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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

5 authors at 2 institutions in 1 country.

Asaf MarcoFaculty of Life Sciences, Gonda Brain Research Center, and asafmarco@gmail.com.
Tatiana KislioukInstitute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel.
Tzlil TabachnikFaculty of Life Sciences, Gonda Brain Research Center, and.
Noam MeiriInstitute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel.
Aron WellerGonda Brain Research Center, and Department of Psychology, Bar Ilan University, Ramat-Gan, Israel; and.
Bar-Ilan University · ILAgricultural Research Organization · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to determine whether epigenetic malprogramming induced by high-fat diet (HFD) has an obesogenic effect on nonmated and mated female rats and their offspring. Further, it aimed to reprogram offspring's epigenetic malprogramming and phenotype by providing normal diet after weaning. Body weight (BW) was measured, and plasma and hypothalamic arcuate nuclei were collected for analysis of hormones, mRNA, and DNA CpG methylation of the promoter of Pomc, a key factor in control of food intake. In nonmated females, HFD decreased Pomc/leptin ratio by ∼38%. This finding was associated with Pomc promoter hypermethylation. While heavier during pregnancy, during lactation HFD dams showed sharper BW decrease (2.5-fold) and loss of Pomc promoter hypermethylation. Moreover, their weight loss was correlated with demethylation (r=-0.707) and with gadd45b mRNA expression levels (r=0.905). Even though offspring of HFD dams ate standard chow from weaning, they displayed increased BW, Pomc promoter hypermethylation, and vulnerability to HFD challenge (3-fold kilocalorie intake increase). These findings demonstrate a long-term effect of maternal HFD on CpG methylation of the Pomc promoter in the offspring, which was not reprogrammed by standard chow from weaning. Further, the results suggest a possible mechanism of demethylation of the Pomc promoter following pregnancy and lactation.

Indexed as

DNA MethylationAdiposityAnimalsAntigens, DifferentiationBody WeightCpG IslandsDiet, High-FatEatingFemaleGADD45 ProteinsGene Expression Regulation, DevelopmentalLactationLeptinMaternal Nutritional Physiological PhenomenaObesityOverweightAntigens, DifferentiationGadd45b protein, ratGADD45 ProteinsLeptinProprotein ConvertasesRNA, Messengerepigeneticsleptinobesity

Identifiers

PMID24928196
PMCPMC5395737
OpenAlexW1976914448

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.