The Hypothalamic–Pituitary–Adrenal–Leptin Axis and Metabolic Health: A Systems Approach to Resilience, Robustness and Control
Open accessAbstract
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.
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The negative correlation on the same experimental dataset was first identified by Aschbacher et al.
“The negative correlation on the same experimental dataset has been first identified by Aschbacher et al. (23).”
From Sparse System Identification of Leptin Dynamics in Women With Obesity (2022) · cites this paper as [23]
Section 3.4 reports an inverse leptin–cortisol association in the study’s data, but only in eight of 18 patients; it does not establish a negative correlation across the whole dataset. The Discussion calls the finding in women with obesity novel, but our copy does not establish that Aschbacher et al. were the first to identify it in this dataset. Page numbers are unavailable in our copy. (LLM, conf=0.79)
Experimental — accuracy not yet measuredLeptin-cortisol dynamics might provide an indirect or functional biomarker of the neuroendocrine starvation response.
“This research further suggests that leptin-cortisol dynamics might provide an indirect or functional biomarker of the neuroendocrine starvation response (23).”
From Sparse System Identification of Leptin Dynamics in Women With Obesity (2022) · cites this paper as [23]
The study was approved by the Medical Ethics Committee of Leiden University.
“The above study was approved by the Medical Ethics Committee of Leiden University (23).”
From Sparse System Identification of Leptin Dynamics in Women With Obesity (2022) · cites this paper as [23]
Aschbacher et al. observed a leptin-cortisol antagonism.
“Aschbacher et al. observed a leptin-cortisol antagonism (23).”
From Sparse System Identification of Leptin Dynamics in Women With Obesity (2022) · cites this paper as [23]
The evidence of a possible negative association is in accordance with previous findings in the correlation-based study by Aschbacher et al.
“The evidence of possible negative association is in accordance with the previous findings in previous correlation based study by Aschbacher et al. (23).”
From Sparse System Identification of Leptin Dynamics in Women With Obesity (2022) · cites this paper as [23]
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- Authors
- Aschbacher, K., Rodriguez-Fernandez, M., van Wietmarschen, H., Tomiyama, A. J., Jain, S., Epel, E., Doyle, F. J., & van der Greef, J.
- Affiliations
- University of California, San Francisco (US)
- University of California, Santa Barbara (US)
- TNO Innovation for Life, Zeist, The Netherlands
- University of California, Los Angeles (US)
- University of California San Diego (US)
- Corresponding author
- Aschbacher, Kirstin
- ORCID
- Venue
- Interface Focus
- Publisher
- The Royal Society
- Published
- 2014-10-06
- Volume
- 4
- Issue
- 5
- Pages
- 20140020
- ISSN
- 2042-8898 (ISSN-L)
- 2042-8901
- PMC
- PMC4142017
- OpenAlex
- W2038209586
- Cited by
- 48
- References
- 72
- Citations by year
- 2026: 6 · 2025: 3 · 2023: 3 · 2022: 7 · 2021: 7 · 2020: 7 · 2019: 5 · 2016: 6 · 2015: 2 · 2014: 2
- FWCI
- 1.64
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Interface Focus (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- TNO Repository (submittedVersion)
- Repository hosted by TU Delft Library (TU Delft) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- hypothalamic-pituitary-adrenal axis, leptin, cortisol, ACTH, obesity, metabolic syndrome, insulin resistance, dynamic system modeling, premenopausal women, fat mass, lean body mass
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