# Modulation of the Inflammatory Response by Adenovirus 36 in Patients with Obesity and Type 2 Diabetes: A Nested Case-Control Study Within a Cohort

**Authors:** Itzae Adonai Gutiérrez-Hurtado, Erika Martínez-López, Manuel Alejandro Rico-Méndez, Karla Mayela Bravo-Villagra, Héctor Eduardo Mendoza-Jaramillo, María del Pilar Sánchez-Rolón, Alejandra Betancourt-Núñez, Martha Patricia Gallegos-Arreola, José Carlos Tapia-Rivera, Andres López-Quintero

PMC · DOI: 10.3390/v17040552 · Viruses · 2025-04-10

## TL;DR

This study explores how Adenovirus 36 affects inflammation and metabolism in people with obesity and diabetes.

## Contribution

The study reveals new insights into how Adenovirus 36 modulates cytokine levels and glucose metabolism in infected individuals.

## Key findings

- HAdV-36 positive individuals had significantly lower IL-6 and higher IL-8 levels.
- They also exhibited lower glucose levels compared to HAdV-36 negative individuals.

## Abstract

Human adenovirus 36 (HAdV-36) is associated with obesity, potentially by promoting adipocyte proliferation and differentiation. Although linked to increased fat storage, HAdV-36 is also correlated with improved insulin sensitivity. Given its potential role in modulating adipose tissue and promoting a less inflammatory metabolic profile, its impacts on pro- and anti-inflammatory cytokine secretion remain unclear. Methods: This nested case-control study compared cytokine levels (IL-10, IL-2, IL-6, IL-8, and TNF-α) between patients with and without HAdV-36 infection. A total of 76 participants were included, with 37 in the control group (HAdV-36 negative) and 39 classified as cases (HAdV-36 positive). Results: HAdV-36 seropositive individuals exhibited significantly lower IL-6 levels and higher IL-8 levels than seronegative participants. Additionally, they had lower glucose levels, suggesting a potential link between HAdV-36 and metabolic regulation. Conclusions: These findings support the hypothesis that HAdV-36 may influence inflammatory and metabolic responses by modulating cytokine expression and glucose levels. Further research is needed to clarify the underlying mechanisms and their implications for metabolic health.

## Linked entities

- **Diseases:** obesity (MONDO:0011122), Type 2 Diabetes (MONDO:0005148)

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, IL2 (interleukin 2) [NCBI Gene 3558] {aka IL-2, TCGF, lymphokine}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** Obesity (MESH:D009765), Inflammatory (MESH:D007249), Type 2 Diabetes (MESH:D003924)
- **Species:** Homo sapiens (human, species) [taxon 9606], Human adenovirus 36 (no rank) [taxon 46936]

## Full text

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## Figures

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## References

40 references — full list in the complete paper: https://tomesphere.com/paper/PMC12030835/full.md

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Source: https://tomesphere.com/paper/PMC12030835