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Cited by 292Ovarian function and disordersGut microbiota and healthDiet, Metabolism, and Disease

The DOI matches its Crossref record; 102 of the 102 references it cites were found in a registry or an index.

Role of gut microbiota in the development of insulin resistance and the mechanism underlying polycystic ovary syndrome: a review

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He, Fang-fang, Li, Yu-mei·2020·Journal of Ovarian Research
DOI 10.1186/s13048-020-00670-3PMC PMC7301991
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Abstract

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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Crossref · 10.1186/s13048-020-00670-3

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Fig. 1 Crosstalk between the gut microbiota and the mammalian host in inflammation and metabolism. The gut microbiota can contribute to host insulin resistance, low-grade inflammation, and hyperandrogenism(HA) through a range of molecular interactions with the host and therefore can indirectly participate in the onset of PCOS
Fig. 1 Crosstalk between the gut microbiota and the mammalian host in inflammation and metabolism. The gut microbiota can contribute to host insulin resistance, low-grade inflammation, and hyperandrogenism(HA) through a range of molecular interactions with the host and therefore can indirectly participate in the onset of PCOSCC BY · PubMed Central
Fig. 2 ①Gut microbiota can cause IR by affecting lipopolysaccharide (LPS) and its receptor CD14(LPS-CD14; ②SCFAs protect intestinal barrier integrity and act on beta cells to promote insulin secretion, thus improving metabolism; ③Bile acids (BAs) are signaling molecules that regulate glucose metabolism and promote insulin sensitivity; ④The metabolic disorder of amino acids might aggravate IR by changing glucose metabolism or inducing inflammation;⑤A vicious cycle between hyperandrogenemia and IR in PCOS, thus promoting the occurrence and development of PCOS; ⑥Gut microbiota and its metabolites cause insulin resistance and hyperinsulinemia by stimulating the secretion of gut-brain peptides and regulating inflammation pathway activation. LPS: lipopolysaccharide; SCFA: short-chain fatty acid; BCAA: branch-chain amino acid; BA: Bile acids
Fig. 2 ①Gut microbiota can cause IR by affecting lipopolysaccharide (LPS) and its receptor CD14(LPS-CD14; ②SCFAs protect intestinal barrier integrity and act on beta cells to promote insulin secretion, thus improving metabolism; ③Bile acids (BAs) are signaling molecules that regulate glucose metabolism and promote insulin sensitivity; ④The metabolic disorder of amino acids might aggravate IR by changing glucose metabolism or inducing inflammation;⑤A vicious cycle between hyperandrogenemia and IR in PCOS, thus promoting the occurrence and development of PCOS; ⑥Gut microbiota and its metabolites cause insulin resistance and hyperinsulinemia by stimulating the secretion of gut-brain peptides and regulating inflammation pathway activation. LPS: lipopolysaccharide; SCFA: short-chain fatty acid; BCAA: branch-chain amino acid; BA: Bile acidsCC BY · PubMed Central

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Research works printed but not linked: 2

  1. Vrieze A, Van Nood E, Holleman F, Salojärvi J, Kootte RS, Bartelsman JFWM, et al. Transfer of Intestinal Microbiota From Lean Donors Increases Insulin Sensitivity in Individuals With Metabolic Syndrome. Gastroenterology. 2012;143(4):913–6.e7. · DOI · Paper page
  2. Chen Fangyuan, LAI Zhiwen, XU Zusen. Analysis of the gut microbial composition in polycystic ovary syndrome with acne. Zigong Maternal and Child Health Hospital. 2019;35(14):2246–51.

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Metadata

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
Publisher
Springer Science and Business Media LLC
Published
2020-06-17
Volume
13
Issue
1
Pages
73-73
ISSN
1757-2215 (ISSN-L)
DOI
10.1186/s13048-020-00670-3
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
FWCI
4.99
Type
journal article
Language
en
Open access
Licence
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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