2 Pathogenesis of IBD Since its emergence in the western world over a century ago, the epidemiology of IBD has undergone a significant shift ( 2.1 Dysbiosis of intestinal flora A reduction in the abundance and diversity of specific bacterial genera in the gut microbiota, as well as alterations in microbiota-derived metabolites, has been identified as a potential key factor in the pathogenesis of IBD ( Roseburia and Phascolarctobacterium , were markedly decreased in UC and CD patients in contrast to healthy people ( Roseburia is known for its role in promoting the generation of gut anti-inflammatory regulatory T cells ( Phascolarctobacterium metabolizes succinate to generate propionate when in co-culture with Paraprevotella ( Phascolarctobacterium populations in IBD patients may impair the production of propionate, thus diminishing the anti-inflammatory effects of SCFAs and contributing to the exacerbation of IBD symptoms
Amsterdam, Elsevier, pp 109118 Arduini A, Gorbunov N, Arrigoni-Martelli E, Dottori S, Molajoni F, Russo F, Federici G
The mechanism of its pathogenesis is not fully understood, multiple parallel hits are believed to be involved, including insulin resistance, hormones secreted from the adipose tissue, nutritional factors, gut microbiota and genetic and epigenetic factors ( In recent years, more and more attention has been paid to intestinal flora and its metabolites
Long-term pioglitazone treatment for patients with nonalcoholic steatohepatitis and prediabetes or type 2 diabetes mellitus: a randomized trial
PLoS ONE 9 , e97330 (2014)
found that TMAO promoted calcium/phosphate-induced calcification in the vascular smooth muscle cells of rats and human urinary system patients in a dose-dependent manner, and upregulated the expression of bone-related molecules (Runt-related transcription factor2, Runx2, and Bone morphogenetic protein-2, BMP2)
