Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMCOpen access

Interplay of obesity and parasitic infection: current evidence of immunogenesis, tumorigenesis and leptin receptor involvement

Saftawy EE., Alghamdi M., Aboulhoda BE.

Narrative Review on Type 2 Diabetes, Chronic Inflammation, published in Nutr Metab (Lond) (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Nutr Metab (Lond) (2025)
Reported sample size
—
Source database
Europe PMC
PMID
40954459
PMCID
PMC12439378
DOI
10.1186/s12986-025-00972-7

Abstract (original English)

Background Parasitic infections possess comparable risk factors to obesity. In addition, obesity impairs innate and adaptive immunity subsequently increasing vulnerability to infectious diseases. Aim The study investigated the leptin/leptin receptors, obesity-parasites mutual relationship and the effect of parasitic infections on immune metabolism, microbiota, and tumorigenesis in the context of obesity. Methodology To implement the current review, articles were gathered using the Egyptian Knowledge Bank (EKB), Web of Science, PubMed, and Google Scholar. Conclusion Leptin enhances anti-parasitic immunity. Obesity favors intestinal colonization of Blastocystis sp., Dientamoeba fragilis, Entamoeba coli, and Giardia intestinalis. Adipocytes act as a niche and a food source for Trypanosoma cruzi, Trypanosoma brucei, and Plasmodium. In addition, Toxoplasma gondii relies on the circulatory cholesterol to thrive. Obesity provokes low-grade chronic inflammation and metabolic syndrome. Yet, Nippostrongylus brasiliensis and Fasciola hepatica attempted to alleviate inflammation and metabolic syndrome. Hookworm improves insulin resistance. However, parasites such as Schistosoma mansoni, Trichuris suis, Taenia pisiformis, Entamoeba histolytica, Trypanosoma cruzi, and Trypanosoma brucei, and Toxoplasma aggravated metabolic immune metabolic syndrome. Obesity hampered immunity against Leishman

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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