Randomized trial examines inulin's effect on inflammation and ADAM17 in atherosclerosis patients, suggesting therapeutic potential.
Objectives This study sought to elucidate the mechanism by which inulin delays atherogenesis, specifically investigating its potential to mitigate inflammation through the inhibition of ADAM17. Methods A cohort of 180 patients (aged 18–75, mean 55 ± 15.4 years) was recruited from Yinchuan Second People’s Hospital (Jan 2021–Jan 2023). Based on carotid artery examinations, participants were stratified into three groups: healthy, plaque-free dyslipidemia (PFD), and atherosclerotic. The following parameters were analyzed: ① serum ADAM17 levels, ② inflammatory markers, and ③ lipid profiles (triglycerides and low-density lipoprotein). Complementary in vitro experiments were conducted to validate the interaction between inulin and ADAM17-mediated inflammatory pathways. Results Serum ADAM17 levels exhibited significant stepwise increases across the patient groups, with marked differences between the healthy, PFD, and atherosclerotic groups (p<0.001). Cellular assays confirmed that inulin administration significantly counteracted the upregulation of IL-1β (p<00.001) induced by ADAM17. Furthermore, IL-6 was found to promote ADAM17 expression, an effect that was significantly suppressed by inulin treatment (p<00.001), demonstrating a clear antagonistic relationship. Conclusions The findings indicate that inulin attenuates atherosclerosis by suppressing ADAM17 expression and its downstream inflammatory cascade. These results provide a strategic insight and a novel perspective for leveraging inflammation suppression to improve patient prognosis.
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Lijuan et al. (2026) studied this question.
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