Evidence map›Paper›PMID 22402988›Full record

ReviewDiabetologia2012

Adipose tissue and fetal programming.

M E Symonds, M Pope, D Sharkey, H Budge

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Diabetologia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06803069 (Investigation of the Mechanisms of the Tendency to Hypothermia in Newborns and Premature Infants During Surgical Interventions and in the Intensive Care Unit), which is not on this map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
–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.

NCT06803069 recruitingnot on this mapstarted 2024, after this paper: background citation

Investigation of the Mechanisms of the Tendency to Hypothermia in Newborns and Premature Infants During Surgical Interventions and in the Intensive Care Unit (Non-Interventional, Single-Center, Prospective Clinical Research)

TypeobservationalSponsorUniversity of PecsRan2024 to 2029Enrolled100ConditionsNeonatal Hypothermia, Brown Adipose Tissue, Preterm and Term Infants, Neonate
3 · Its place in the literature

Who cites it

64 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
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  7. Review
  8. Review
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  16. Impact of maternalFrontiers in immunology · 2024
    Article
  17. Article
  18. CFTR regulates brown adipocyte thermogenesis via the cAMP/PKA signaling pathway.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2023
    Article
  19. Article
  20. Review

4 more citing papers are in PubMed but not listed here.

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.

M E SymondsThe Early Life Nutrition Research Unit, Academic Division of Child Health, School of Clinical Sciences, University Hospital, Nottingham, NG7 2UH, UK. michael.symonds@nottingham.ac.uk
M Pope
D Sharkey
H Budge

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adipose tissue function changes with development. In the newborn, brown adipose tissue (BAT) is essential for ensuring effective adaptation to the extrauterine environment, and its growth during gestation is largely dependent on glucose supply from the mother to the fetus. The amount, location and type of adipose tissue deposited can also determine fetal glucose homeostasis. Adipose tissue first appears at around mid-gestation. Total adipose mass then increases through late gestation, when it comprises a mixture of white and brown adipocytes. BAT possesses a unique uncoupling protein, UCP1, which is responsible for the rapid generation of large amounts of heat at birth. Then, during postnatal life some, but not all, depots are replaced by white fat. This process can be utilised to investigate the physiological conversion of brown to white fat, and how it is re-programmed by nutritional changes in pre- and postnatal environments. A reduction in early BAT deposition may perpetuate through the life cycle, thereby suppressing energy expenditure and ultimately promoting obesity. Normal fat development profiles in the offspring are modified by changes in maternal diet at defined stages of pregnancy, ultimately leading to adverse long-term outcomes. For example, excess macrophage accumulation and the onset of insulin resistance occur in an adipose tissue depot-specific manner in offspring born to mothers fed a suboptimal diet from early to mid-gestation. In conclusion, the growth of the different fetal adipose tissue depots varies according to maternal diet and, if challenged in later life, this can contribute to insulin resistance and impaired glucose homeostasis.

Indexed as

Adipose Tissue, BrownAdipose Tissue, WhiteAnimalsFemaleFetal DevelopmentHumansInsulin ResistanceModels, BiologicalPregnancy

Identifiers

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.