Publications by authors named "C Rosiers"

Elevated numbers of atherogenic lipoproteins (apoB) predict the incidence of type 2 diabetes (T2D). We reported that this may be mediated via the activation of the NLRP3 inflammasome, as low-density lipoproteins (LDL) induce interleukin-1 beta (IL-1β) secretion from human white adipose tissue (WAT) and macrophages. However, mitigating nutritional approaches remained unknown.

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The inflammatory bowel diseases (IBD) known as Crohn's disease (CD) and ulcerative colitis (UC) are chronic inflammatory diseases of the gastrointestinal tract believed to arise because of an imbalance between the epithelial, immune and microbial systems. It has been shown that biological differences (genetic, epigenetic, microbial, environmental, etc.) exist between patients with IBD, with multiple risk factors been associated with disease susceptibility and IBD-related phenotypes (e.

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  • Myo-inositol is elevated in patients with heart failure (HF), particularly in those with heart failure with preserved ejection fraction (HFpEF), and is associated with negative clinical outcomes.
  • The study measured plasmatic myo-inositol levels in large cohorts from Belgium and Canada, revealing significant increases in HF patients compared to those without.
  • Elevated myo-inositol levels correlate with worsening kidney function and cardiac markers, suggesting a potential role in the development and progression of HFpEF.
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  • Metabolite genome-wide association studies (mGWAS) help uncover how genetics influence metabolite levels, but interpreting these associations is tough without effective tools.
  • The authors introduce a new metric called shortest reactional distance (SRD) from the KEGG database to improve the biological interpretation of mGWAS results.
  • Their research shows that SRD values correlate well with mGWAS findings and can help identify potential false negatives in existing metabolic pathway databases, making SRD a valuable tool for linking genetics to metabolism.
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Cardiomyopathy is a major complication of thalassemia, yet the precise underlying molecular mechanisms remain unclear. We examined whether altered lipid metabolism is an early driving factor in the development of cardiomyopathy using the Th3/+ mouse model of thalassemia. At age 20 weeks, male and female Th3/+ mice manifested anemia and iron overload; however, only males displayed metabolic defects and altered cardiac function.

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