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• W3097585142 abstract "Infl ammatory bowel disease (IBD) has been in the researchers’ focus of attention for at least two decades and is one of the most studied human pathologies. On the one hand, advances in scientifi c knowledge about the pathophysiology of IBD have contributed to the development of new drugs. But on the other hand, the etiology of these diseases remains unknown. And we have the right to call IBD “the mystery of modern gastroenterology”. Obviously, the increase in the number of patients with ulcerative colitis (UC) and Crohn’s disease (CD) occurs simultaneously with the change in lifestyle and basic approaches to nutrition in modern society, the so-called “Western lifestyle”. IBD became more common around the same time that the obesity pandemic began. At fi rst glance, the relationship between IBD and obesity can be questioned. However, with a detailed analysis of predisposing factors and the prevalence of these diseases, many common features can be found. Obesity is becoming more common among patients with IBD and plays an important role both in development and in progress of UC and CD. It has been argued that adipocytes, release of pro-infl ammatory cytokines, imbalance of leptin and adiponectin, decrease in mucin synthesis, induction of intestinal permeability, bacterial translocation are involved in the pathogenesis of IBD. Changes in the composition of the intestinal microbiota are probably an important pathogenetic link between obesity and IBD. We present this review to physicians and gastroenterologists for information purposes, focusing on studies conducted over the past years. Literature was searched in PubMed and Google Scholar using the following Keywords: ulcerative colitis, obesity, colonic microbiota, leptin, adiponectin." @default.
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• W3097585142 date "2020-10-30" @default.
• W3097585142 modified "2023-09-27" @default.
• W3097585142 title "Obesity and infl ammatory bowel disease: is there a link?" @default.
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• W3097585142 doi "https://doi.org/10.31146/1682-8658-ecg-182-10-133-141" @default.
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