ArticleMolecular medicine (Cambridge, Mass.)2010
Changes in the expression of insulin signaling pathway molecules in endometria from polycystic ovary syndrome women with or without hyperinsulinemia.
Article in Molecular medicine (Cambridge, Mass.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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.
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.
Who cites it
35 citing papers in PubMed, 100 citations in OpenAlex.
- Endometrial shedding effect on conception and live birth in women with polycystic ovary syndrome.Obstetrics and gynecology · 2012Trial
- Advances in the Study of Endometrial Receptivity and Glucose Metabolism Mechanisms in Insulin Resistance.Endocrinology, diabetes & metabolism · 2026Review
- LncPVT1 modulates decidualization and links to recurrent spontaneous abortions via glucose and lipid metabolic regulation.Scientific reports · 2026Article
- Molecular Impact of Metabolic and Endocrine Disturbance on Endometrial Function in Polycystic Ovary Syndrome.International journal of molecular sciences · 2025Review
- Interplay between elevated RAB5B gene expression and insulin resistance among women with PCOS-insights from a case-control study.Endocrine · 2025Article
- The Interplay of Uterine Health and Obesity: A Comprehensive Review.Biomedicines · 2024Review
- The role of immunity in insulin resistance in patients with polycystic ovary syndrome.Frontiers in endocrinology · 2024Review
- Advances in the study of the correlation between insulin resistance and infertility.Frontiers in endocrinology · 2024Review
- Endometrial Glucose Metabolism During Early Pregnancy.Reproduction & fertility · 2023Article
- The Effect of Metformin and Carbohydrate-Controlled Diet on DNA Methylation and Gene Expression in the Endometrium of Women with Polycystic Ovary Syndrome.International journal of molecular sciences · 2023Article
- Regulatory mechanisms of HMGB1 and its receptors in polycystic ovary syndrome-driven gravid uterine inflammation.The FEBS journal · 2023Article
- Exploring the relationship between osteoporosis and polycystic ovary syndrome based on bioinformatics.Medicine · 2022Article
- Metformin Treatment Regulates the Expression of Molecules Involved in Adiponectin and Insulin Signaling Pathways in Endometria from Women with Obesity-Associated Insulin Resistance and PCOS.International journal of molecular sciences · 2022Article
- Article
- Metformin and Insulin Resistance: A Review of the Underlying Mechanisms behind Changes in GLUT4-Mediated Glucose Transport.International journal of molecular sciences · 2022Review
- Development and validation of dietary and lifestyle insulinemic indices among Iranian adult population.Nutrition & metabolism · 2022Article
- Research Progress on the Mechanism Between Polycystic Ovary Syndrome and Abnormal Endometrium.Frontiers in physiology · 2021Review
- Endometrial Glucose Transporters in Health and Disease.Frontiers in cell and developmental biology · 2021Review
- Hyperandrogenic Milieu Dysregulates the Expression of Insulin Signaling Factors and Glucose Transporters in the Endometrium of Patients With Polycystic Ovary Syndrome.Reproductive sciences (Thousand Oaks, Calif.) · 2020Article
- Hyperinsulinemia: An Early Indicator of Metabolic Dysfunction.Journal of the Endocrine Society · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystic ovary syndrome (PCOS) is an endocrine-metabolic disorder associated with insulin resistance and compensatory hyperinsulinemia. Scarce information is available on the expression of molecules involved in the insulin pathway in endometria from women with PCOS. Therefore, we examined the protein levels of insulin-signaling molecules, like insulin receptor, insulin-receptor substrate (IRS)-1, pIRS-1Y612, Akt, AS160, pAS160T642 and GLUT4 in endometria from PCOS women with or without hyperinsulinemia. Protein levels were assessed by Western blot and immunohistochemistry in 21 proliferative-phase endometria from control women (CE = 7), normoinssulinemic PCOS women (PCOSE-NI = 7) and hyperinsulinemic PCOS women (PCOSE-HI = 7). The data show no differences in the expression of insulin receptor between all groups as assessed by Western blot; however, IRS-1 and pIRS-1Y612 were lower in PCOSE-HI than controls and PCOSE-NI (P < 0.05). AS160 was detected in all analyzed tissues with similar expression levels between groups. Importantly, PCOSE-HI exhibited lower levels of pAS160T642 (P < 0.05) and of GLUT4 (P < 0.05) compared with CE. The immunohistochemistry for insulin receptor, IRS-1, Akt, AS160 and GLUT4 showed epithelial and stromal localization; IRS-1 staining was lower in PCOSE-HI (P < 0.05). In conclusion, human endometrium has the machinery for glucose uptake mediated by insulin. The diminished expression of GLUT4, as well as the lower level of pIRS-1Y612 and pAS160T642 exhibited by PCOSE-HI, suggests a disruption in the translocation of vesicles with GLUT4 to the cell surface in these patients.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.