# Association of Systemic Inflammation with Inflammatory mRNA Expression in Visceral Adipose Tissue in Gestational Diabetes

**Authors:** Renata Saucedo, María Isabel Peña-Cano, Mary Flor Díaz-Velázquez, Alejandra Contreras-Ramos, Miranda Moleres-Orduña, Debbie López-Sánchez, Jorge Valencia-Ortega, Javier Pérez-Duran

PMC · DOI: 10.3390/metabo15100644 · Metabolites · 2025-09-26

## TL;DR

This study finds that gestational diabetes is linked to higher systemic inflammation and altered inflammatory gene expression in visceral fat.

## Contribution

The study identifies specific immune cell ratios and inflammatory gene expression changes in visceral adipose tissue in gestational diabetes.

## Key findings

- Women with GDM had higher NLR, MLR, and VAT TNF-α/IL-10 mRNA ratios compared to NGT women.
- Monocyte and eosinophil counts correlated with VAT inflammatory gene expression in GDM patients.

## Abstract

Background/Objectives: Gestational diabetes mellitus (GDM) is characterized by a systemic inflammatory response and the expression of inflammatory factors in visceral adipose tissue (VAT). However, the association between these two inflammatory processes has not been fully elucidated. Therefore, this study aimed to (1) investigate whether whole blood counts, the neutrophil–lymphocyte ratio (NLR), the monocyte–lymphocyte ratio (MLR), serum adiponectin levels, and the mRNA expression of inflammatory genes (TLR2, TLR4, pro-inflammatory cytokines: IL-1β, IL-6, and TNF-α, anti-inflammatory cytokines: IL-1RA, IL-10, and adiponectin) in VAT are altered in women with GDM in comparison to pregnant women with normal glucose tolerance (NGT), and (2) determine the correlations between systemic and local VAT inflammation in all, GDM, and NGT women. Methods: Study of 50 GDM and 50 women with NGT with a cross-sectional design. Standard biochemical and hematological tests were conducted and relative mRNA expression in VAT was measured by RT-qPCR. Results: Women with GDM showed higher neutrophil, monocyte, NLR, MLR, and VAT TNF-α/IL-10 mRNA expression ratios while lymphocyte and eosinophil counts, serum adiponectin, and mRNA local VAT inflammatory markers such as TLR2, TLR4, IL-1β, IL-6, IL-1RA, and IL-10 were lower in women with GDM relative to women with NGT. Additionally, the circulating monocyte count were associated with TLR2 and TLR-4 VAT mRNA expression levels and eosinophils count were associated with IL-1β, IL-6, IL-10, and IL-1RA VAT expression levels in women with GDM. Conclusions: GDM is characterized by systemic inflammation, and some circulating immune cells, such as monocytes and eosinophils, are associated with the expression of inflammatory markers in VAT.

## Linked entities

- **Genes:** TLR2 (toll like receptor 2) [NCBI Gene 7097], TLR4 (toll like receptor 4) [NCBI Gene 7099], IL1B (interleukin 1 beta) [NCBI Gene 3553], IL6 (interleukin 6) [NCBI Gene 3569], TNF (tumor necrosis factor) [NCBI Gene 7124], IL1R1 (interleukin 1 receptor type 1) [NCBI Gene 3554], IL10 (interleukin 10) [NCBI Gene 3586]
- **Diseases:** Gestational diabetes mellitus (MONDO:0005406)

## Full-text entities

- **Genes:** IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, IL1RN (interleukin 1 receptor antagonist) [NCBI Gene 3557] {aka CRMO2, DIRA, ICIL-1RA, IL-1RN, IL-1ra, IL-1ra3}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, TLR2 (toll like receptor 2) [NCBI Gene 7097] {aka CD282, TIL4}, TLR4 (toll like receptor 4) [NCBI Gene 7099] {aka ARMD10, CD284, TLR-4, TOLL}, ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}
- **Diseases:** GDM (MESH:D016640), Inflammation (MESH:D007249)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

52 references — full list in the complete paper: https://tomesphere.com/paper/PMC12565992/full.md

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Source: https://tomesphere.com/paper/PMC12565992