Role of gut microbiota in the development of insulin resistance and the mechanism underlying polycystic ovary syndrome: A review
Open accessAbstract
Polycystic ovary syndrome (PCOS) is a complex endocrine and metabolic disorder. Typically, it is characterized by hirsutism, hyperandrogenism, ovulatory dysfunction, menstrual disorders and infertility. To date, its pathogenesis remains unclear. However, insulin resistance (IR) is considered as the primary pathological basis for its reproductive dysfunction. On the other hand, a condition in which insulin is over-secreted is called hyperinsulinemia. IR/Hyperinsulinemia is associated with chronic inflammation, hormonal changes, follicular dysplasia, endometrial receptivity changes, and abortion or infertility. Additionally, it increases incidence of complications during pregnancy and has been associated with anxiety, depression, and other psychological disorders. Gut microbiota, the “second genome” acquired by the human body, can promote metabolism, immune response through interaction with the external environment. Gut microbiota dysbiosis can cause IR, which is closely linked to the occurrence of PCOS. This article reviewed recent findings on the roles of gut microbiota in the development of insulin resistance and the mechanism underlying polycystic ovary syndrome.
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Lifestyle-induced changes in the gastrointestinal tract microbiome are a significant factor in the etiology of PCOS.
“Lifestyle-induced changes in the gastrointestinal tract microbiome are another significant factor in the etiology of PCOS [52,53].”
From Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment (2022) · cites this paper as [53]
The Introduction describes a proposed pathway in which obesity or a high-sugar, high-fat, low-fiber diet alters gut flora and may contribute to PCOS. “The treatment approach in PCOS” likewise says dietary changes alter gut flora and high-sugar foods may induce PCOS through that pathway. The review supports the proposed link, but does not establish lifestyle-induced microbiome changes as a significant causal factor in PCOS etiology. (LLM, conf=0.87)
Experimental — accuracy not yet measuredDiet-related changes in the gastrointestinal microbiome have been shown to cause insulin resistance in women with PCOS.
“As discussed in the dysbiosis section, diet-related changes in the gastrointestinal microbiome have also been shown to cause IR in women with PCOS [53,55].”
From Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment (2022) · cites this paper as [53]
The Introduction describes a proposed pathway from diet-related gut dysbiosis to insulin resistance, and “The treatment approach in PCOS” says high-sugar foods may trigger that pathway. Neither passage establishes that diet-related microbiome changes have been shown to cause insulin resistance in women with PCOS; the causal microbiome experiment the review describes was in mice. Page numbers are not available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredInsulin resistance can be caused by a wide variety of mechanisms that disrupt any part of the metabolic signaling system, including autoantibodies, receptor agonists and antagonists, hormones, inflammatory cytokines, oxidative stress, nutrient sensors and metabolic intermediates.
“Insulin resistance can be caused by a wide variety of mechanisms that have the ability to disrupt any part of this metabolic signaling system [53,161]. These include autoantibodies, receptor agonists and antagonists, hormones, inflammatory cytokines, oxidative stress, nutrient sensors and metabolic intermediates [160,161,162,163].”
From Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment (2022) · cites this paper as [53]
The sections “Gut microbiome contributes to insulin resistance” and “Endotoxemia” describe inflammatory mediators reducing insulin sensitivity and immune activation interfering with insulin receptor function. “Gut-brain peptides” also links gut hormones and metabolites to insulin resistance. The paper does not substantiate the full list of mechanisms, particularly autoantibodies, receptor agonists and antagonists, oxidative stress, and nutrient sensors, or the claim that they can disrupt any part of the signaling system. No page numbers are available in our copy. (LLM, conf=0.86)
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- Authors
- He, F.-F., & Li, Y.-M.
- Affiliations
- Central South University (CN)
- Corresponding author
- Li, Yu-mei
- ORCID
- Li, Yu-mei
- Venue
- Journal of Ovarian Research
- Published
- 2020-06-17
- Volume
- 13
- Issue
- 1
- Pages
- 73-73
- ISSN
- 1757-2215 (ISSN-L)
- PMC
- PMC7301991
- OpenAlex
- W3036640353
- Cited by
- 289
- References
- 102
- Citations by year
- 2026: 41 · 2025: 50 · 2024: 62 · 2023: 57 · 2022: 48 · 2021: 28 · 2020: 2 · 2018: 1
- FWCI
- 4.99
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Ovarian Research (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Ovarian function and disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Keywords
- gut microbiota, polycystic ovary syndrome, insulin resistance, hyperinsulinemia, dysbiosis, chronic inflammation, reproductive disorders, infertility, hyperandrogenism, pregnancy complications, anxiety and depression
- MeSH terms
- Gastrointestinal Microbiome, Animals, Female, Humans, Insulin Resistance, Polycystic Ovary Syndrome, Mice
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