Evaluation of the Relationship Between Insulin-like Growth Factor-1 Levels, Systemic Immune-Inflammatory Markers, and Metabolic Comorbidities in Patients with Obesity
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Le résumé fourni par la source
Background: Insulin-like growth factor-1 (IGF-1) plays a role in metabolism and immune regulation. Although obesity is associated with chronic inflammation, the relationship between IGF-1 levels and systemic inflammatory markers remains unclear. This study aimed to examine the association between IGF-1 levels, systemic inflammation, and metabolic comorbidities in individuals with obesity. Methods: This retrospective cross-sectional study included 214 adults with a BMI ≥35 kg/m 2 evaluated between June 2019 and March 2025. Participants were classified as low IGF-1 (standard deviation score [SDS] ≤ −2.0) or standard IGF-1 (−2.0 < SDS < 2.0). Clinical and laboratory data were analyzed, including neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio, lymphocyte-to-monocyte ratio, systemic immune-inflammation index (SII), systemic inflammation response index, and systemic inflammation aggregate index. Results: Low IGF-1 was identified in 8.88% of patients. No differences were found between groups regarding diabetes, dyslipidemia, or hypertension. NLR (2.21 vs. 1.79; p = 0.005) and SII (614.6 vs. 521.8; p = 0.041) were significantly higher in the standard IGF-1 group. SII was positively correlated with systolic blood pressure, alanine aminotransferase, and insulin. IGF-1 SDS was not correlated with inflammatory markers. Conclusions: Lower IGF-1 levels were not associated with higher systemic inflammation. These findings highlight the heterogeneity of inflammatory responses in obesity and suggest the need for further research.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Evaluation of the Relationship Between Insulin-like Growth Factor-1 Levels, Systemic Immune-Inflammatory Markers, and Metabolic Comorbidities in Patients with Obesity
- Date Crossref
- 03/06/2026
- Éditeur
- SAGE Publications
- Type
- journal-article
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