| Autor: |
Colston JM; Division of Infectious Diseases and International Health, University of Virginia School of Medicine, Charlottesville, Virginia., Chen YT; Department of Emergency Medicine, Chi-Mei Medical Center, Tainan, Taiwan., Hinson P; College of Arts and Sciences, University of Virginia, Charlottesville, Virginia., Nguyen NH; College of Arts and Sciences, University of Virginia, Charlottesville, Virginia., Peñataro Yori P; Division of Infectious Diseases and International Health, University of Virginia School of Medicine, Charlottesville, Virginia., Olortegui MP; Asociación Benéfica Prisma, Unidad de Investigaciones Biomédicas, Iquitos, Peru., Rengifo Trigoso D; Asociación Benéfica Prisma, Unidad de Investigaciones Biomédicas, Iquitos, Peru., Siguas Salas M; Asociación Benéfica Prisma, Unidad de Investigaciones Biomédicas, Iquitos, Peru., Guerrant RL; Division of Infectious Diseases and International Health, University of Virginia School of Medicine, Charlottesville, Virginia.; Center for Global Health Equity, University of Virginia School of Medicine, Charlottesville, Virginia., François R; School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina., Kosek MN; Division of Infectious Diseases and International Health, University of Virginia School of Medicine, Charlottesville, Virginia.; Division of Public Health Sciences, University of Virginia School of Medicine, Charlottesville, Virginia. |
| Abstrakt: |
Metabolic syndrome is a cluster of risk factors for cardiovascular disease afflicting more than 1 billion people worldwide and is increasingly being identified in younger age groups and in socioeconomically disadvantaged settings in the global south. Enteropathogen exposure and environmental enteropathy in infancy may contribute to metabolic syndrome by disrupting the metabolic profile in a way that is detectable in cardiometabolic markers later in childhood. A total of 217 subjects previously enrolled in a birth cohort in Amazonian Peru were monitored annually from ages 2 to 5 years. A total of 197 blood samples collected in later childhood were analyzed for 37 cardiometabolic biomarkers, including adipokines, apolipoproteins, cytokines, which were matched to extant early-life markers of enteropathy ascertained between birth and 2 years. Multivariate and multivariable regression models were fitted to test for associations, adjusting for confounders. Fecal and urinary markers of intestinal permeability and inflammation (myeloperoxidase, lactulose, and mannitol) measured in infancy were associated with later serum concentrations of soluble CD40-ligand, a proinflammatory cytokine correlated with adverse metabolic outcomes. Fecal myeloperoxidase was also associated with later levels of omentin-1. Enteric protozoa exposure showed stronger associations with later cardiometabolic markers than viruses, bacteria, and overall diarrheal episodes. Early-life enteropathy markers were associated with altered adipokine, apolipoprotein, and cytokine profiles later in childhood consistent with an adverse cardiometabolic disease risk profile in this cohort. Markers of intestinal permeability and inflammation measured in urine (lactulose, mannitol) and stool (myeloperoxidase, protozoal infections) during infancy may predict metabolic syndrome in adulthood. |
