# Distribution of prolactin and its correlation with insulin resistance in women with polycystic ovary syndrome

**Authors:** Stefan Ghobrial, Robert Krysiak, Tal Goldstein, Antonella Patsch, Chiara Paternostro, Florian Heinzl, Rodrig Marculescu, Johannes Ott

PMC · DOI: 10.3389/fendo.2025.1674795 · Frontiers in Endocrinology · 2025-10-01

## TL;DR

This study finds that higher prolactin levels are linked to lower insulin resistance in women with polycystic ovary syndrome, regardless of their specific PCOS type.

## Contribution

The study identifies a novel inverse relationship between prolactin and insulin resistance in PCOS and reveals metabolic subtypes through clustering.

## Key findings

- Prolactin levels were similar across PCOS phenotypes, but phenotype D had lower insulin resistance prevalence.
- Prolactin was inversely correlated with insulin resistance in all PCOS groups.
- Cluster analysis identified three distinct metabolic subtypes independent of PCOS phenotypes.

## Abstract

Polycystic ovary syndrome (PCOS) is often associated with insulin resistance (IR). The role of prolactin (PRL) in this context remains unclear, particularly across different PCOS phenotypes. The aim of this study was to investigate the distribution of PRL, as well as its correlation with basal IR in women with PCOS.

200 women with PCOS, evenly distributed across phenotypes A-D and matched for age and body mass index (BMI) were retrospectively analyzed. PRL, Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), sexual hormone binding globulin (SHBG), testosterone, and BMI were assessed. Correlation analysis and unsupervised clustering (based on PRL and HOMA-IR) were performed.

PRL levels were similar across phenotypes, but phenotype D had a significantly lower prevalence of HOMA-IR ≥ 2.5 (p = 0.032). PRL was inversely correlated with HOMA-IR in all groups (p < 0.05). Cluster analysis identified three distinct subgroups, independent of phenotype, differing significantly in both PRL and HOMA-IR.

PRL is inversely associated with IR in PCOS, regardless of phenotype. Cluster analysis reveals metabolic subtypes not captured by current phenotype-based classification, suggesting potential for improved risk stratification.

## Linked entities

- **Proteins:** PROLACTIN (PROLACTIN protein)
- **Diseases:** polycystic ovary syndrome (MONDO:0008487)

## Full-text entities

- **Genes:** PRL (prolactin) [NCBI Gene 5617] {aka GHA1, pPRL}, SHBG (sex hormone binding globulin) [NCBI Gene 6462] {aka ABP, SBP, TEBG}
- **Diseases:** PCOS (MESH:D011085), IR (MESH:D007333)
- **Chemicals:** testosterone (MESH:D013739)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12520901/full.md

## References

36 references — full list in the complete paper: https://tomesphere.com/paper/PMC12520901/full.md

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Source: https://tomesphere.com/paper/PMC12520901