# Maternal Obesity Modulates Postpartum Inflammatory and Hormonal Profiles, Without Detectable Differences in Tested Redox Markers

**Authors:** Juliana Augusta Dias, Isabela Carvalho Guimarães, Vinícius Lopes Cantuária, Bruna Oliveira Costa, Joyce Mirlane Moreira Costa, Bruna Caroline Chaves Garcia, Juliane Duarte Santos, Lourdes Fernanda Godinho, Marina Luiza Baêta Costa, Etel Rocha‐Vieria, Marco Fabrício Dias‐Peixoto, Kinulpe Honorato‐Sampaio

PMC · DOI: 10.1111/aji.70227 · American Journal of Reproductive Immunology · 2026-03-17

## TL;DR

Maternal obesity affects postpartum inflammation and hormones but not redox markers, suggesting a unique immune response in obese mothers after childbirth.

## Contribution

The study reveals distinct postpartum inflammatory and hormonal profiles in obese mothers, with no differences in redox markers.

## Key findings

- CRP levels increased postpartum only in obese mothers, indicating heightened inflammation.
- IL-6 levels declined postpartum only in non-obese mothers.
- No differences in oxidative stress markers were found between obese and non-obese groups.

## Abstract

Maternal obesity is associated with elevated inflammatory markers, hormonal dysregulation, and metabolic disturbances. However, how maternal obesity modulates systemic inflammatory, hormonal, and redox profiles in the peripartum and postpartum periods remains incompletely understood.

This observational study evaluated inflammatory biomarkers, steroid hormone levels, and oxidative stress markers in obese (n = 8) and non‐obese (n = 11) pregnant women undergoing labor induction. Peripheral maternal blood samples were collected immediately before induction and again within approximately 5–10 mins after delivery. Placental tissue was collected postpartum within the same interval. Comparative analyses between groups and time points were performed using repeated‐measures statistical models.

C‐reactive protein (CRP) levels increased postpartum only in the obese group, indicating an enhanced inflammatory response after delivery. In contrast, interleukin‐6 (IL‐6) levels declined postpartum only in the non‐obese group. No between‐group differences were detected in the oxidative stress markers assessed, either in maternal blood or placental tissue.

Maternal obesity is associated with distinct postpartum inflammatory and hormonal profiles, characterized by sustained CRP elevation and altered cytokine dynamics. No between‐group differences were detected in the redox markers assessed, suggesting preserved redox balance in the parameters evaluated. These findings highlight the importance of considering postpartum immune modulation in obese parturients and support further investigation into obesity‐associated inflammatory regulation during the peripartum period.

## Linked entities

- **Proteins:** IL6 (interleukin 6)
- **Diseases:** obesity (MONDO:0011122)

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, SOD1 (superoxide dismutase 1) [NCBI Gene 6647] {aka ALS, ALS1, HEL-S-44, IPOA, SOD, STAHP}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, CAT (catalase) [NCBI Gene 847], INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}
- **Diseases:** metabolic dysregulation (MESH:D021081), hyperinsulinemia (MESH:D006946), preterm birth (MESH:D047928), Maternal (MESH:D000079262), infarcted (MESH:D007238), Obese (MESH:D009765), type 2 diabetes (MESH:D003924), dystocia (MESH:D004420), pain (MESH:D010146), immune dysfunction (MESH:D007154), cardiovascular disease (MESH:D002318), mitochondrial dysfunction (MESH:D028361), hyperlipidemia (MESH:D006949), fetal distress (MESH:D005316), preeclampsia (MESH:D011225), metabolic (MESH:D008659), overweight (MESH:D050177), cancer (MESH:D009369), immune dysregulation (OMIM:614878), hypertrophy (MESH:D006984), metabolic disturbances (MESH:D024821), gestational diabetes (MESH:D016640), macrosomia (MESH:D005320), Inflammation (MESH:D007249), adiposity (MESH:D018205), congenital anomalies (MESH:D000013)
- **Chemicals:** 2',7'-dichlorodihydrofluorescein diacetate (MESH:C110400), DCF (MESH:C037631), BKY (-), TBARS (MESH:D017392), O (MESH:D010100), heparin (MESH:D006493), oxytocin (MESH:D010121), Progesterone (MESH:D011374), EDTA (MESH:D004492), lipid (MESH:D008055), misoprostol (MESH:D016595), DCFH-DA (MESH:C029569), ROS (MESH:D017382), estradiol (MESH:D004958), NO (MESH:D009614), Steroid hormones (MESH:D013256), estriol (MESH:D004964), nitrogen (MESH:D009584)
- **Species:** Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

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## References

53 references — full list in the complete paper: https://tomesphere.com/paper/PMC12993264/full.md

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Source: https://tomesphere.com/paper/PMC12993264