Evidence map›Paper›PMID 27108813›Full record

ArticleInternational journal of obesity (2005)2016

DNA methylation regulates hypothalamic gene expression linking parental diet during pregnancy to the offspring's risk of obesity in Psammomys obesus.

I Khurana, A Kaspi, M Ziemann, T Block, T Connor, B Spolding, A Cooper, P Zimmet, A El-Osta, K Walder

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Article in International journal of obesity (2005), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
4.6field-weighted citation impact, top 6% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

I KhuranaEpigenetics in Human Health and Disease Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
A KaspiEpigenetics in Human Health and Disease Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
M ZiemannEpigenetics in Human Health and Disease Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
T BlockEpigenetics in Human Health and Disease Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
T ConnorMetabolic Research Unit, Faculty of Health, Medicine, Nursing and Behavioural Sciences, Deakin University, Waurn Ponds, Victoria, Australia.
B SpoldingMetabolic Research Unit, Faculty of Health, Medicine, Nursing and Behavioural Sciences, Deakin University, Waurn Ponds, Victoria, Australia.
A CooperMetabolic Research Unit, Faculty of Health, Medicine, Nursing and Behavioural Sciences, Deakin University, Waurn Ponds, Victoria, Australia.
P ZimmetEpigenetics in Human Health and Disease Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
A El-OstaEpigenetics in Human Health and Disease Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
K WalderMetabolic Research Unit, Faculty of Health, Medicine, Nursing and Behavioural Sciences, Deakin University, Waurn Ponds, Victoria, Australia.
Baker Heart and Diabetes Institute · AUDeakin University · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectiveThe rising incidence of obesity is a major public health issue worldwide. Recent human and animal studies suggest that parental diet can influence fetal development and is implicated with risk of obesity and type 2 diabetes in offspring. The hypothalamus is central to body energy homoeostasis and appetite by controlling endocrine signals. We hypothesise that offspring susceptibility to obesity is programmed in the hypothalamus in utero and mediated by changes to DNA methylation, which persist to adulthood. We investigated hypothalamic genome-wide DNA methylation in Psammomys obesus diet during pregnancy to the offspring's risk of obesity.

methodsUsing methyl-CpG binding domain capture and deep sequencing (MBD-seq), we examined the hypothalamus of offspring exposed to a low-fat diet and standard chow diet during the gestation and lactation period.

resultsOffspring exposed to a low-fat parental diet were more obese and had increased circulating insulin and glucose levels. Methylome profiling identified 1447 genomic regions of differential methylation between offspring of parents fed a low-fat diet compared with parents on standard chow diet. Pathway analysis shows novel DNA methylation changes of hypothalamic genes associated with neurological function, nutrient sensing, appetite and energy balance. Differential DNA methylation corresponded to changes in hypothalamic gene expression of Tas1r1 and Abcc8 in the offspring exposed to low-fat parental diet.

conclusionSubject to parental low-fat diet, we observe DNA methylation changes of genes associated with obesity in offspring.

Indexed as

Fetal DevelopmentGene Expression RegulationAnimalsDiabetes Mellitus, Type 2Diet, Fat-RestrictedDisease Models, AnimalDNA MethylationFemaleGerbillinaeHypothalamusLactationMaternal Nutritional Physiological PhenomenaObesityPregnancyPrenatal Exposure Delayed Effects

Identifiers

PMID27108813
OpenAlexW2343673478

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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.