Evidence map›Paper›PMID 31351130›Full record

ArticleBiochimica et biophysica acta. Molecular basis of disease2019

Maternal obesity impairs fetal mitochondriogenesis and brown adipose tissue development partially via upregulation of miR-204-5p.

Hanning Wang, Yanting Chen, Xueying Mao, Min Du

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta. Molecular basis of disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Childhood obesity from the genes to the epigenome.Frontiers in endocrinology · 2024
    Review
  4. Obesity in children: inheritance and treatment - state of art 2024.Pediatric endocrinology, diabetes, and metabolism · 2024
    Article
  5. Early life impacts of maternal obesity: a window of opportunity to improve the health of two generations.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Epigenetic contribution to obesity.Mammalian genome : official journal of the International Mammalian Genome Society · 2020
    Review
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 at 2 institutions in 2 countries.

Hanning WangBeijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, Beijing 100194, China; College of Food Science & Nutritional Engineering, China Agricultural University, Beijing 100083, China.
Yanting ChenLaboratory of Nutrigenomics and Growth Biology, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA.
Xueying MaoBeijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, Beijing 100194, China; College of Food Science & Nutritional Engineering, China Agricultural University, Beijing 100083, China.
Min DuBeijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, Beijing 100194, China; Laboratory of Nutrigenomics and Growth Biology, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA. Electronic address: min.du@wsu.edu.
China Agricultural University · CNWashington State University · US

Funding

Maternal obesity, AMPK and fetal brown adipogenesisR01HD067449 · NICHD · WASHINGTON STATE UNIVERSITY · PI MIN DU · 2010 to 2026
$4.6M
NICHD NIH HHS R01 HD067449
6 · The paper itself

Abstract

Maternal obesity (MO) predisposes offspring to metabolic disorders, but the mechanisms remain poorly defined. Recent studies emphasize the importance of brown adipose tissue (BAT) in maintaining metabolic health, and MO was recently demonstrated to impair BAT thermogenic function in offspring. The current study aimed to investigate the mechanisms leading to the impairment in fetal BAT development due to MO. Female C57BL/6J mice were fed a control diet or a 60% high-fat diet for 10 weeks, mated and maintained on their respective diets during pregnancy. Fetal tissue was collected at E18.5, the late stage of pregnancy. Fetal BAT contained more triglycerides compared to the control, which was correlated with higher expression of white adipogenic markers. On the other hand, the expression of BAT markers was down-regulated in the MO fetal BAT. Based on RNA-sequencing analyses, genes related to mitochondriogenesis and myogenesis were found to be down-regulated, while those related to white adipocyte differentiation were up-regulated in MO fetal BAT. Because brown adipocytes are derived from myogenic progenitors, the down-regulation of myogenic genes might partially explain hampered brown adipogenesis in MO fetal BAT. Consistently, mitochondrial DNA and mitochondrial biogenesis markers were also down-regulated in MO fetal BAT. MicroRNA-sequencing identified that miR-204-5p expression was elevated in MO fetal BAT. This microRNA targeted the 3'-untranslated regions of PGC1α and Sirt1 mRNA to suppress their expression and impair mitochondriogenesis. In summary, MO impaired fetal BAT development through suppressing myogenesis and brown adipogenesis while enhancing white adipogenic commitment, and inhibited mitochondriogenesis partially through enhancing miR-204-5p expression.

Indexed as

3' Untranslated RegionsAdipose Tissue, BrownAdipose Tissue, WhiteAnimalsDiet, High-FatDown-RegulationFemaleMiceMice, Inbred C57BLMicroRNAsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPregnancyPregnancy in ObesitySirtuin 1ThermogenesisUp-Regulation3' Untranslated RegionsMicroRNAsMIRN205 microRNA, mousePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseSirt1 protein, mouseSirtuin 1Brown adipose tissueFetusMaternal obesitymiR-204-5pMitochondriogenesis

Identifiers

PMID31351130
PMCPMC6708788
OpenAlexW2964023949

What OpenQuestion holds

Textmetadata
LicenceTDM
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.