# The Role of Melatonin in the Inflammatory Process in Patients with Hyperglycemia and Leishmania Infection

**Authors:** Thalissa Mariana de Moraes Martins, Felipe Rubin Ferrari, Adriele Ataides de Queiroz, Letícia Damas Leão Dalcin, Danielle Cristina Honorio França, Adenilda Cristina Honório-França, Eduardo Luzía França, Danny Laura Gomes Fagundes-Triches

PMC · DOI: 10.3390/biom14080950 · Biomolecules · 2024-08-06

## TL;DR

This study explores how melatonin affects inflammation in diabetic patients with leishmaniasis, finding altered levels of melatonin and inflammatory markers.

## Contribution

The study investigates melatonin's role in the inflammatory process in patients with both hyperglycemia and leishmaniasis, a rarely studied combination.

## Key findings

- Leishmaniasis patients showed significantly increased TNF-α and decreased melatonin levels.
- Diabetic patients with leishmaniasis had higher melatonin levels than the control group.
- TNF-α may influence melatonin production in leishmaniasis, contributing to inflammation.

## Abstract

Type 2 diabetes mellitus is a metabolic disorder that causes chronic high blood sugar levels, and diabetic patients are more susceptible to infections. American cutaneous leishmaniasis is an infectious disease caused by a parasite that affects the skin and mucous membranes, leading to one or multiple ulcerative lesions. Chronic inflammation and functional changes in various organs and systems, including the immune system, are the primary causes of both diseases. Melatonin, an essential immunomodulatory, antioxidant, and neuroprotective agent, can benefit many immunological processes and infectious diseases, including leishmaniasis. Although, limited reports are available on diabetic patients with leishmaniasis. The literature suggests that melatonin may play a promising role in inflammatory disorders. This study was designed to assess melatonin levels and inflammatory mediators in diabetic patients affected by leishmaniasis. Blood samples from 25 individuals were analyzed and divided into four groups: a control group (without any diseases), a Leishmania-positive group, patients with type 2 diabetes mellitus, and patients with a combination of both diseases. This study measured the serum levels of melatonin through ELISA, while IL-4 and TNF-α were measured using flow cytometry, and C-reactive protein was measured through turbidimetry. This study found that patients with leishmaniasis significantly increased TNF-α and decreased melatonin levels. However, the group of diabetic patients with leishmaniasis showed higher melatonin levels than the control group. These observations suggest that TNF-α may influence melatonin production in patients with American cutaneous leishmaniasis, potentially contributing to the inflammatory characteristics of both diseases.

## Linked entities

- **Proteins:** IL4 (interleukin 4), TNF (tumor necrosis factor)
- **Diseases:** Type 2 diabetes mellitus (MONDO:0005148), American cutaneous leishmaniasis (MONDO:0005859), leishmaniasis (MONDO:0011989)

## Full-text entities

- **Genes:** IL4 (interleukin 4) [NCBI Gene 3565] {aka BCGF-1, BCGF1, BSF-1, BSF1, IL-4}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}
- **Diseases:** Type 2 diabetes mellitus (MESH:D003924), Leishmania Infection (MESH:D007896), Chronic inflammation (MESH:D007249), infectious diseases (MESH:D003141), ulcerative lesions (MESH:D014456), disease (MESH:D004194), metabolic disorder (MESH:D008659), Hyperglycemia (MESH:D006943), diabetic (MESH:D003920), American cutaneous leishmaniasis (MESH:D016773)
- **Chemicals:** blood sugar (MESH:D001786), Melatonin (MESH:D008550)
- **Species:** Homo sapiens (human, species) [taxon 9606], Leishmania (subgenus) [taxon 38568]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11352828/full.md

## References

73 references — full list in the complete paper: https://tomesphere.com/paper/PMC11352828/full.md

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Source: https://tomesphere.com/paper/PMC11352828