Evidence map›Paper›PMID 24549139›Full record

ArticleInternational journal of obesity (2005)2014

Adipocyte morphology and implications for metabolic derangements in acquired obesity.

S Heinonen, L Saarinen, J Naukkarinen, A Rodríguez, G Frühbeck, A Hakkarainen, J Lundbom, N Lundbom, K Vuolteenaho, E Moilanen and 6 more

Abstract readTwin Study
PubMed Publisher
In one paragraph

Article in International journal of obesity (2005), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 3 pooled it
7.5field-weighted citation impact, top 2% 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

67 citing papers in PubMed, 3 syntheses or guidelines pooled it, 144 citations in OpenAlex.

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  10. EndoBridge 2024: pearls and highlights.Hormones (Athens, Greece) · 2025
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7 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

16 authors at 7 institutions in 3 countries.

S HeinonenObesity Research Unit, Research Programs Unit, Diabetes and Obesity, University of Helsinki, Helsinki, Finland.
L SaarinenResearch Programs Unit, Genome-Scale Biology and Institute of Biomedicine, Biochemistry and Developmental Biology, Helsinki, Finland.
J Naukkarinen1] Obesity Research Unit, Research Programs Unit, Diabetes and Obesity, University of Helsinki, Helsinki, Finland [2] FIMM, Institute for Molecular Medicine, University of Helsinki, Helsinki, Finland.
A RodríguezMetabolic Research Laboratory, Clinica Universidad de Navarra, & CIBERobn, Instituto de Salud Carlos III, Pamplona, Spain.
G FrühbeckMetabolic Research Laboratory, Clinica Universidad de Navarra, & CIBERobn, Instituto de Salud Carlos III, Pamplona, Spain.
A HakkarainenHelsinki Medical Imaging Center, University of Helsinki, Helsinki, Finland.
J LundbomHelsinki Medical Imaging Center, University of Helsinki, Helsinki, Finland.
N LundbomHelsinki Medical Imaging Center, University of Helsinki, Helsinki, Finland.
K VuolteenahoThe Immunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, Tampere, Finland.
E MoilanenThe Immunopharmacology Research Group, University of Tampere School of Medicine and Tampere University Hospital, Tampere, Finland.
P ArnerLipid Laboratory, Department of Medicine, Karolinska University Hospital Huddinge, Karolinska Institutet, Stockholm, Sweden.
S HautaniemiResearch Programs Unit, Genome-Scale Biology and Institute of Biomedicine, Biochemistry and Developmental Biology, Helsinki, Finland.
A SuomalainenResearch Program of Molecular Neurology and Department of Neurology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.
J Kaprio1] FIMM, Institute for Molecular Medicine, University of Helsinki, Helsinki, Finland [2] Finnish Twin Cohort Study, Department of Public Health, Hjelt Institute, University of Helsinki, Helsinki Finland [3] National Institute for Health and Welfare, Department of Mental Health and Substance Abuse Services, Helsinki, Finland.
A RissanenDepartment of Psychiatry, Helsinki University Central Hospital, Helsinki, Finland.
K H Pietiläinen1] Obesity Research Unit, Research Programs Unit, Diabetes and Obesity, University of Helsinki, Helsinki, Finland [2] FIMM, Institute for Molecular Medicine, University of Helsinki, Helsinki, Finland [3] Department of Medicine, Division of Endocrinology, Helsinki University Central Hospital, Helsinki, Finland.
University of Helsinki · FIHelsinki University Hospital · FIClinica Universidad de Navarra · ESInstituto de Salud Carlos III · ESKarolinska Institutet · SETampere University · FITampere University Hospital · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAdipocyte size and number have been suggested to predict the development of metabolic complications in obesity. However, the genetic and environmental determinants behind this phenomenon remain unclear.

methodsWe studied this question in rare-weight discordant (intra-pair difference (Δ) body mass index (BMI) 3-10 kg m(-2), n=15) and concordant (ΔBMI 0-2 kg m(-)(2), n=5) young adult (22-35 years) monozygotic twin pairs identified from 10 birth cohorts of Finnish twins (n=5 500 pairs). Subcutaneous abdominal adipocyte size from surgical biopsies was measured under a light microscope. Adipocyte number was calculated from cell size and total body fat (D × A).

resultsThe concordant pairs were remarkably similar for adipocyte size and number (intra-class correlations 0.91-0.92, P<0.01), suggesting a strong genetic control of these measures. In the discordant pairs, the obese co-twins (BMI 30.6 ± 0.9 kg m(-2)) had significantly larger adipocytes (volume 547 ± 59 pl), than the lean co-twins (24.9 ± 0.9 kg m(-)(2); 356 ± 34 pl, P<0.001). In 8/15 pairs, the obese co-twins had less adipocytes than their co-twins. These hypoplastic obese twins had significantly higher liver fat (spectroscopy), homeostatic model assessment-index, C-reactive protein and low-density lipoprotein cholesterol than their lean co-twins. Hyperplastic obesity was observed in the rest (7/15) of the pairs, obese and lean co-twins having similar metabolic measures. In all pairs, Δadipocyte volume correlated positively and Δcell number correlated negatively with Δhomeostatic model assessment-index and Δlow-density lipoprotein, independent of Δbody fat. Transcripts most significantly correlating with Δadipocyte volume were related to a reduced mitochondrial function, membrane modifications, to DNA damage and cell death.

conclusionsTogether, hypertrophy and hypoplasia in acquired obesity are related to metabolic dysfunction, possibly through disturbances in mitochondrial function and increased cell death within the adipose tissue.

Indexed as

MetabolomeTwins, MonozygoticAdipocytesAdipose TissueAdultBody Mass IndexBody WeightEnergy MetabolismFemaleFinlandGene-Environment InteractionGene ExpressionGenetic Predisposition to DiseaseHumansLongitudinal StudiesMale

Identifiers

PMID24549139
OpenAlexW2024392277

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.