Adiponectin and Altered Metabolic Signalling in Asymptomatic Malaria: A Community-Based, Cross-Sectional Study of Nigerian Children

Abstract

Background: Asymptomatic Plasmodium falciparum infection is common among school-aged children in endemic communities. Whether a microscopy-detectable infection is accompanied by a clinically important disturbance of adipocytokine signalling in apparently well children remains uncertain.

Objective: To determine whether microscopy-detectable asymptomatic Plasmodium falciparum infection is associated with changes in circulating adiponectin, leptin, resistin and the leptin-to-adiponectin ratio among afebrile Nigerian school-aged children.

Methods: A community-based, cross-sectional study was conducted among afebrile, symptom-screen-negative children aged 5-9 years, recruited from 20 public primary schools in Southwest Nigeria between March and June 2024. Malaria status was determined by microscopy of Giemsa-stained thick and thin blood films. Plasma adiponectin, leptin and resistin levels were measured by duplicate enzyme-linked immunosorbent assay, and the leptin-to-adiponectin ratio was calculated. Log-transformed outcomes were analysed using multivariable linear regression with school-level cluster-robust standard errors.

Results: Overall, 106/317 children (33.4%) had microscopy-detectable malaria. Baseline characteristics were broadly comparable, although malaria-positive children had lower mean weight-for-age z-scores. In the fully adjusted model, malaria positivity was not independently associated with adiponectin (-2.4%; 95% CI -10.9 to 6.9), leptin (-2.9%; 95% CI -11.4 to 6.4), resistin (2.1%; 95% CI -13.4 to 20.5) or the leptin-to-adiponectin ratio (-0.5%; 95% CI -11.2 to 11.4). Among malaria-positive children with parasite density data, adiponectin showed a weak positive monotonic association with parasite density (Spearman's rho = 0.31; p = 0.002).

Conclusion: Binary microscopy-defined asymptomatic malaria was not associated with major adipocytokine disruption. Parasite burden may carry a weak adiponectin signal, but the finding is hypothesis-generating and requires longitudinal studies using molecular parasite detection and fuller inflammatory-metabolic phenotyping.