Ovarian hormones and obesity

Leeners, Brigitte; Geary, Nori; Tobler, Philippe N.; Asarian, Lori

doi:10.1093/humupd/dmw045

Cited by 407Regulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic DiseasesMenopause: Health Impacts and Treatments

Ovarian hormones and obesity

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Leeners, Brigitte, Geary, Nori, Tobler, Philippe N., Asarian, Lori·2017·Human Reproduction Update

DOI 10.1093/humupd/dmw045PMC PMC5850121

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Abstract

BACKGROUND: Obesity is caused by an imbalance between energy intake, i.e. eating and energy expenditure (EE). Severe obesity is more prevalent in women than men worldwide, and obesity pathophysiology and the resultant obesity-related disease risks differ in women and men. The underlying mechanisms are largely unknown. Pre-clinical and clinical research indicate that ovarian hormones may play a major role. OBJECTIVE AND RATIONALE: We systematically reviewed the clinical and pre-clinical literature on the effects of ovarian hormones on the physiology of adipose tissue (AT) and the regulation of AT mass by energy intake and EE. SEARCH METHODS: Articles in English indexed in PubMed through January 2016 were searched using keywords related to: (i) reproductive hormones, (ii) weight regulation and (iii) central nervous system. We sought to identify emerging research foci with clinical translational potential rather than to provide a comprehensive review. OUTCOMES: We find that estrogens play a leading role in the causes and consequences of female obesity. With respect to adiposity, estrogens synergize with AT genes to increase gluteofemoral subcutaneous AT mass and decrease central AT mass in reproductive-age women, which leads to protective cardiometabolic effects. Loss of estrogens after menopause, independent of aging, increases total AT mass and decreases lean body mass, so that there is little net effect on body weight. Menopause also partially reverses women's protective AT distribution. These effects can be counteracted by estrogen treatment. With respect to eating, increasing estrogen levels progressively decrease eating during the follicular and peri-ovulatory phases of the menstrual cycle. Progestin levels are associated with eating during the luteal phase, but there does not appear to be a causal relationship. Progestins may increase binge eating and eating stimulated by negative emotional states during the luteal phase. Pre-clinical research indicates that one mechanism for the pre-ovulatory decrease in eating is a central action of estrogens to increase the satiating potency of the gastrointestinal hormone cholecystokinin. Another mechanism involves a decrease in the preference for sweet foods during the follicular phase. Genetic defects in brain α-melanocycte-stimulating hormone-melanocortin receptor (melanocortin 4 receptor, MC4R) signaling lead to a syndrome of overeating and obesity that is particularly pronounced in women and in female animals. The syndrome appears around puberty in mice with genetic deletions of MC4R, suggesting a role of ovarian hormones. Emerging functional brain-imaging data indicates that fluctuations in ovarian hormones affect eating by influencing striatal dopaminergic processing of flavor hedonics and lateral prefrontal cortex processing of cognitive inhibitory controls of eating. There is a dearth of research on the neuroendocrine control of eating after menopause. There is also comparatively little research on the effects of ovarian hormones on EE, although changes in ovarian hormone levels during the menstrual cycle do affect resting EE. WIDER IMPLICATIONS: The markedly greater obesity burden in women makes understanding the diverse effects of ovarian hormones on eating, EE and body adiposity urgent research challenges. A variety of research modalities can be used to investigate these effects in women, and most of the mechanisms reviewed are accessible in animal models. Therefore, human and translational research on the roles of ovarian hormones in women's obesity and its causes should be intensified to gain further mechanistic insights that may ultimately be translated into novel anti-obesity therapies and thereby improve women's health.

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The mechanisms behind the hormonal regulation of adipose tissue distribution are complex and still incompletely characterized, but may arise from effects on lipolysis and lipogenesis, adipocyte differentiation, and insulin sensitivity.
“Although the mechanisms behind the hormonal regulation of AT distribution are complex and still incompletely characterized, they may arise from effects on lipolysis and lipogenesis, adipocyte differentiation, and insulin sensitivity [9,24,[28][29][30].”
From Adipose tissue estrogen production and metabolism in premenopausal women (2021) · cites this paper as [9]
In “Puberty and young adulthood” (pp. 10–11), the paper describes regional fat distribution in terms of fatty-acid uptake, triglyceride synthesis, lipolysis, and sex-dependent adipocyte differentiation, while saying hormonal and genetic interactions are only beginning to be understood. “Simple Obesity” (p. 16) discusses decreased insulin sensitivity as a consequence of expanded adipose depots, not as a proposed mechanism by which hormones regulate their distribution. (LLM, conf=0.86)
Experimental — accuracy not yet measured
The typical female adipose tissue distribution, concentrated in subcutaneous and femoro-gluteal regions, is estrogen-mediated.
“The typical female AT distribution, with an emphasis in the subcutaneous and femoro-gluteal regions, is estrogen-mediated [9].”
From Adipose tissue estrogen production and metabolism in premenopausal women (2021) · cites this paper as [9]
The development and regulation of the different fat depots in the female body are controlled by complex interactions between adipose tissue genes and ovarian hormones.
“The development and regulation of the different fat depots in the female body are controlled by complex interactions between AT genes and ovarian hormones [9].”
From Adipose tissue estrogen production and metabolism in premenopausal women (2021) · cites this paper as [9]

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Adipose tissue estrogen production and metabolism in premenopausal women
Hetemäki, N., Mikkola, T. S., Tikkanen, M. J., Wang, F., Hämäläinen, E., Turpeinen, U., Haanpää, M., Vihma, V., & Savolainen-Peltonen, H. (2021) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2021.105849 · Cited by 111 · see citing works
“The typical female AT distribution, with an emphasis in the subcutaneous and femoro-gluteal regions, is estrogen-mediated [9].”
Obesity: pathophysiology and therapeutic interventions
Kong, Y., Yang, H., Nie, R., Zhang, X., Zuo, F., Zhang, H., & Nian, X. (2025) · Molecular Biomedicine · doi:10.1186/s43556-025-00264-9 · Cited by 89 · see citing works

Authors: Leeners, B., Geary, N., Tobler, P. N., & Asarian, L.
Affiliations: University of Zurich (CH)
Cornell University (US)
Corresponding author: Leeners, Brigitte
ORCID: Leeners, Brigitte
Geary, Nori
Tobler, Philippe N.
Asarian, Lori
Venue: Human Reproduction Update
Publisher: Oxford University Press (OUP)
Published: 2017-03-02
Volume: 23
Issue: 3
Pages: 300-321
ISSN: 1355-4786 (ISSN-L)
1460-2369
DOI: 10.1093/humupd/dmw045
PMC: PMC5850121
OpenAlex: W2605240544
Semantic Scholar: 97ccbcf1d27228a104df64dc823748df268df67e
Cited by: 407
References: 317
Citations by year: 2026: 40 · 2025: 50 · 2024: 52 · 2023: 54 · 2022: 77 · 2021: 49 · 2020: 43 · 2019: 27 · 2018: 13 · 2017: 2
FWCI: 1.48
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Human Reproduction Update (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
RERO DOC (Universität Bern) (submittedVersion)
Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
Zurich Open Repository and Archive (University of Zurich)
Funders: National Institutes of Health (DK 092608)
Swiss NSF (PP00P1_150739, 00014_165884)
Philhuman Stiftung, Lichtenstein
Topics: Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Menopause: Health Impacts and Treatments
Keywords: ovarian hormones, female obesity, estrogen, progestins, energy balance, body fat distribution, menopause, appetite regulation, menstrual cycle, cholecystokinin, melanocortin-4 receptor, binge eating, sweet food preference, striatal dopamine, neuroimaging, body weight regulation, estrogen therapy, energy expenditure, sex differences in obesity
MeSH terms: Adipose Tissue, Age Factors, Animals, Eating, Estrogens, Female, Humans, Menopause, Menstrual Cycle, Obesity, Progesterone, Sexual Maturation, Women's Health

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