Evidence map›Paper›PMID 25285198›Full record

ArticleInterface focus2014

The hypothalamic-pituitary-adrenal-leptin axis and metabolic health: a systems approach to resilience, robustness and control.

Kirstin Aschbacher, Maria Rodriguez-Fernandez, Herman van Wietmarschen, A Janet Tomiyama, Shamini Jain, Elissa Epel, Francis J Doyle, Jan van der Greef

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Interface focus, 2014. 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
1.3field-weighted citation impact, top 23% 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, 43 citations in OpenAlex.

  1. Review
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  11. Depression and Cardiovascular Disease: The Viewpoint of Platelets.International journal of molecular sciences · 2020
    Review
  12. Article
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  15. Review
  16. Article
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  18. The role of leptin in regulating bone metabolism.Metabolism: clinical and experimental · 2015
    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

8 authors at 5 institutions in 2 countries.

Kirstin AschbacherDepartment of Psychiatry , University of California , San Francisco, CA , USA ; The Institute for Integrative Health , Baltimore, MD , USA.ORCID 0000-0001-6191-6432
Maria Rodriguez-FernandezDepartment of Chemical Engineering , University of California , Santa Barbara, CA , USA.ORCID 0000-0002-8598-5229
Herman van WietmarschenTNO Innovation for Life , Zeist , The Netherlands ; Department of Analytical Biosciences , Leiden University , Leiden , The Netherlands.
A Janet TomiyamaDepartment of Psychology , University of California , Los Angeles, CA , USA.ORCID 0000-0002-2152-5813
Shamini JainDepartment of Brain, Mind & Healing , Samueli Institute , Alexandria, VA , USA ; Department of Psychiatry , University of California , San Diego, CA , USA.
Elissa EpelDepartment of Psychiatry , University of California , San Francisco, CA , USA.ORCID 0000-0002-9334-4720
Francis J DoyleDepartment of Chemical Engineering , University of California , Santa Barbara, CA , USA.ORCID 0000-0001-5342-4083
Jan van der GreefTNO Innovation for Life , Zeist , The Netherlands ; Department of Analytical Biosciences , Leiden University , Leiden , The Netherlands.
Leiden University · NLUniversity of California, San Francisco · USUniversity of California, Santa Barbara · USUniversity of California, Los Angeles · USUniversity of California San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoids contribute to obesity and metabolic syndrome; however, the mechanisms are unclear, and prognostic measures are unavailable. A systems level understanding of the hypothalamic-pituitary-adrenal (HPA)-leptin axis may reveal novel insights. Eighteen obese premenopausal women provided blood samples every 10 min over 24 h, which were assayed for cortisol, adrenocorticotropin releasing hormone (ACTH) and leptin. A published personalized HPA systems model was extended to incorporate leptin, yielding three parameters: (i) cortisol inhibitory feedback signalling, (ii) ACTH-adrenal signalling, and (iii) leptin-cortisol antagonism. We investigated associations between these parameters and metabolic risk profiles: fat and lean body mass (LBM; using dual-energy X-ray absorptiometry), and insulin resistance. Decreased cortisol inhibitory feedback signalling was significantly associated with greater fat (kg; p = 0.01) and insulin resistance (p = 0.03) but not LBM. Leptin significantly antagonized cortisol dynamics in eight women, who exhibited significantly lower 24 h mean leptin levels, LBM and higher ACTH-adrenal signalling nocturnally (all p < 0.05), compared with women without antagonism. Traditional neuroendocrine measures did not predict metabolic health, whereas a dynamic systems approach revealed that lower central inhibitory cortisol feedback signalling was significantly associated with greater metabolic risk. While exploratory, leptin-cortisol antagonism may reflect a 'neuroendocrine starvation' response.

Indexed as

dynamic systemsmetabolic syndromeobesitypsychological stressrobustnessstress-eating

Identifiers

PMID25285198
PMCPMC4142017
OpenAlexW2038209586

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.