Evidence map›Paper›PMID 27917127›Full record

ArticleFrontiers in physiology2016

Maternal High Fat Diet Alters Skeletal Muscle Mitochondrial Catalytic Activity in Adult Male Rat Offspring.

Chantal A Pileggi, Christopher P Hedges, Stephanie A Segovia, James F Markworth, Brenan R Durainayagam, Clint Gray, Xiaoyuan D Zhang, Matthew P G Barnett, Mark H Vickers, Anthony J R Hickey and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 45 citations in OpenAlex.

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  9. High-fat diet during pregnancy promotes fetal skeletal muscle fatty acid oxidation and insulin resistance in an ovine model.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
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  19. Frontiers in physiology · 2021
    Article
  20. SMN Depleted Mice Offer a Robust and Rapid Onset Model of Nonalcoholic Fatty Liver Disease.Cellular and molecular gastroenterology and hepatology · 2021
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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

12 authors at 2 institutions in 2 countries.

Chantal A PileggiLiggins Institute, University of Auckland Auckland, New Zealand.
Christopher P HedgesCollege of Sport and Exercise Science, Institute of Sport, Exercise and Active Living, Victoria UniversityMelbourne, VIC, Australia; Applied Surgery and Metabolism Laboratory, School of Biological Sciences, University of AucklandAuckland, New Zealand.
Stephanie A SegoviaLiggins Institute, University of AucklandAuckland, New Zealand; Gravida: National Centre for Growth and Development, University of AucklandAuckland, New Zealand.
James F MarkworthLiggins Institute, University of Auckland Auckland, New Zealand.
Brenan R DurainayagamLiggins Institute, University of Auckland Auckland, New Zealand.
Clint GrayLiggins Institute, University of AucklandAuckland, New Zealand; Gravida: National Centre for Growth and Development, University of AucklandAuckland, New Zealand.
Xiaoyuan D ZhangLiggins Institute, University of AucklandAuckland, New Zealand; Gravida: National Centre for Growth and Development, University of AucklandAuckland, New Zealand.
Matthew P G BarnettFood Nutrition and Health Team, Food and Bio-based Products Group, AgResearch Grasslands Palmerston North, New Zealand.
Mark H VickersLiggins Institute, University of AucklandAuckland, New Zealand; Gravida: National Centre for Growth and Development, University of AucklandAuckland, New Zealand.
Anthony J R HickeyApplied Surgery and Metabolism Laboratory, School of Biological Sciences, University of Auckland Auckland, New Zealand.
Clare M ReynoldsLiggins Institute, University of AucklandAuckland, New Zealand; Gravida: National Centre for Growth and Development, University of AucklandAuckland, New Zealand.
David Cameron-SmithLiggins Institute, University of Auckland Auckland, New Zealand.
University of Auckland · NZAgResearch · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A maternal high-fat (HF) diet during pregnancy can lead to metabolic compromise, such as insulin resistance in adult offspring. Skeletal muscle mitochondrial dysfunction is one mechanism contributing to metabolic impairments in insulin resistant states. Therefore, the present study aimed to investigate whether mitochondrial dysfunction is evident in metabolically compromised offspring born to HF-fed dams. Sprague-Dawley dams were randomly assigned to receive a purified control diet (CD; 10% kcal from fat) or a high fat diet (HFD; 45% kcal from fat) for 10 days prior to mating, throughout pregnancy and during lactation. From weaning, all male offspring received a standard chow diet and soleus muscle was collected at day 150. Expression of the mitochondrial transcription factors nuclear respiratory factor-1 (NRF1) and mitochondrial transcription factor A (mtTFA) were downregulated in HF offspring. Furthermore, genes encoding the mitochondrial electron transport system (ETS) respiratory complex subunits were suppressed in HF offspring. Moreover, protein expression of the complex I subunit, NDUFB8, was downregulated in HF offspring (36%), which was paralleled by decreased maximal catalytic linked activity of complex I and III (40%). Together, these results indicate that exposure to a maternal HF diet during development may elicit lifelong mitochondrial alterations in offspring skeletal muscle.

Indexed as

developmental programmingmaternal high fatmitochondriaskeletal muscle

Identifiers

PMID27917127
PMCPMC5114294
OpenAlexW2553046043

What OpenQuestion 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 OpenQuestion graph.