Abstract
We tested the hypothesis that a particular immune activation profile might be correlated with insulin resistance in a general population. By measuring 43 markers of immune, endothelial, and coagulation activation, we have previously shown that five different immune activation profiles may be distinguished in 150 volunteers. One of these profiles, Profile 2, characterized by CD4+ T cell senescence, inflammation, monocyte, B cell, and endothelial activation, presented elevated insulinemia, glycemia, triglyceridemia, and γ-glutamyl transferase, a marker of liver injury, in comparison with other profiles. Our data are compatible with a model in which a particular immune activation profile might favor the development of insulin resistance and metabolic syndrome. In this hypothesis, identification of this profile, that is feasible with only 3 markers with an error rate of 5%, might allow to personalize the screening and prevention of metabolic syndrome-driven morbidities as liver steatosis.
Highlights
We tested the hypothesis that a particular immune activation profile might be correlated with insulin resistance in a general population
A specific immune activation profile is linked to insulin resistance and metabolic syn‐ drome
We tested to see whether one of the immune activation (IA) profiles we had observed in the 150 subjects we have previously analyzed was associated with insulin resistance (IR) and Metabolic Syndrome (MetS)
Summary
We tested the hypothesis that a particular immune activation profile might be correlated with insulin resistance in a general population. Our data are compatible with a model in which a particular immune activation profile might favor the development of insulin resistance and metabolic syndrome In this hypothesis, identification of this profile, that is feasible with only 3 markers with an error rate of 5%, might allow to personalize the screening and prevention of metabolic syndrome-driven morbidities as liver steatosis. We have recently shown, using 43 cell surface and soluble markers, that distinct IA profiles may be distinguished by a double hierarchical clustering in 150 people aged 55–69 years who were visiting a health center for routine check-up[5] Some of these profiles were linked to potential causes of IA as a low level of regulatory T cells, a CD4+ T cell subpopulation able to downregulate IA, or microbial translocation[5].
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