Abstract
Micronutrient deficiencies are common in inflammatory bowel disease and have clinical impact, being both a sign of complicated disease and a cause of morbidity. The involved systemic inflammatory response is responsible for altering the concentration of a wide range of trace elements in the serum, including zinc and selenium. This review summarizes recent advances and evidence-based knowledge regarding the impact of selenium and zinc on oxidative stress and microbiota changes in IBD patients. Getting new insight into the impact of malnutrition, particularly on the micronutrients' impact on the development, composition, and metabolism of microbiota, as well as the influence of oxidative stress and the mucosal immune response, could help in implementing new management strategies for IBD patients, with focus on a more integrated approach.
Highlights
Inflammatory bowel disease (IBD) has been the focus of basic science and translational-clinical research, resulting in the exponential growth of knowledge regarding its predisposing factors, possible cause(s), and underlying cellular and molecular mechanisms
Given the significant role of zinc and selenium deficiency in determining poor outcome for IBD patients, which suggests that these micronutrients could be potential therapeutic candidates for IBD, this review will focus on various pathophysiological manners in which micronutrient deficiency could result in impaired evolution of IBD patients and how research into these mechanisms could impact IBD therapy
This outcome could be interceded: it is plausible that under supplemented Se status the disease activity would be significantly decreased. This effect could be mediated through several pathways, including the upregulation of PPARγ, which acts as inhibitor of NF-κB activation in various cell types, such as intestinal epithelial cells, macrophages, and dendritic cells, influencing the production of proinflammatory cytokines, involved in the pathology of IBD [66]
Summary
Inflammatory bowel disease (IBD) has been the focus of basic science and translational-clinical research, resulting in the exponential growth of knowledge regarding its predisposing factors, possible cause(s), and underlying cellular and molecular mechanisms. There is pathophysiological background for micronutrient deficit during inflammation, especially in the suppression of carrier proteins synthesis in the liver, due to proinflammatory cytokines; this leads to the sequestration of some trace elements in the liver as a consequence of the inflammatory response. This type of deficiency is common at diagnosis, obviously due to impaired absorption, but may persist throughout the course of the disease due to various factors, such as poor intake in the context of restrictive diet, direct intestinal loss, or a hypercatabolic state in IBD patients. Given the significant role of zinc and selenium deficiency in determining poor outcome for IBD patients, which suggests that these micronutrients could be potential therapeutic candidates for IBD, this review will focus on various pathophysiological manners in which micronutrient deficiency could result in impaired evolution of IBD patients and how research into these mechanisms could impact IBD therapy
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
