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Nutritional Immunology and Inflammation/Immunometabolism (Oral Session 15)

(OR15-05-25) Circulating Immune Cell Metabolism Is Associated With Body Mass Index and Insulin Resistance in Children and Adolescents

Monday, June 2, 2025
2:48 PM - 3:00 PM ET
Location: S230 CD

    Presenting Author(s)

  • Shannon Rose, PhD (she/her/hers)

    Associate Professor
    University of Tennessee Health Science Center College of Nursing
    Memphis, Tennessee, United States

    Disclosure(s): No relevant financial relationship(s) with ineligible companies to disclose.

    • Co-Author(s)

  • RL

    Reid D. Landes, PhD

    University of Arkansas for Medical Sciences
    Little Rock, Arkansas, United States

  • ET

    Emir Tas

    University of Pittsburg School of Medicine, United States

  • EB

    Elisabet Børsheim, PhD

    University of Arkansas for Medical Sciences
    Little Rock, Arkansas, United States

Objectives: Obesity-associated inflammation drives insulin resistance (IR) and the development of type 2 diabetes and emerges early, even in young children. Therapeutically targeting immune cell metabolism could combat inflammation. We aimed to understand how bioenergetics of peripheral blood mononuclear cells (PBMCs) change upon ex vivo stimulation with anti-CD3/anti-CD28. We hypothesized that these bioenergetic changes differ in children based on obesity status and insulin sensitivity.

Methods: This cross-sectional study included 46 children aged 8–17 years. Body mass index (BMI) and BMIz were determined using CDC growth charts. IR was estimated using the homeostatic model assessment of insulin resistance (HOMA-IR), calculated as (fasting glucose [mg/dL] × fasting insulin [µIU/mL])/405. Isolated PBMCs were cultured for 40 hours with or without anti-CD3/anti-CD28 Dynabeads (1 bead/cell) to induce stimulation. ATP production rates from mitochondrial respiration (mitoATP) and glycolysis (glycoATP) were measured using the Seahorse XFe96 analyzer. Spearman correlations evaluated associations between PBMC bioenergetics, BMI z-scores, and HOMA-IR.

Results: Total ATP production rate (mitoATP + glycoATP) in unstimulated PBMCs positively correlated with BMIz (r = 0.304, p = 0.040) and HOMA-IR (r = 0.312, p = 0.035). No significant correlations were observed between stimulated PBMC bioenergetics and BMIz or HOMA-IR. Weak negative associations were noted between HOMA-IR and stimulation-induced changes in mitoATP (r = -0.220, p = 0.141) and total ATP production rate (r = -0.214, p = 0.152).

Conclusions: In children, higher BMIz and HOMA-IR are linked to increased ATP production in resting PBMCs, suggesting potential metabolic activation of circulating immune cells. Investigating the mechanisms driving this metabolically activated state and its contribution to chronic inflammation could offer critical insights into strategies for reducing inflammation and enhancing metabolic health in children with obesity.

Funding Sources: NIGMS, Arkansas Children’s Research Institute, Arkansas Biosciences Institute, and USDA/ARS