Investigating the Impact of Obesity on Intestinal Health: A Report

This report investigates the relationship between obesity and the function of the intestinal barrier, highlighting its impact on inflammatory bowel disease (IBD). The study details how obesity leads to metabolic alterations, specifically insulin resistance and glucose intolerance, which in turn contribute to low-grade systemic inflammation. This inflammation is associated with dysfunction of the intestinal barrier, often triggered by lipopolysaccharide (LPS) from the gut microbiota, particularly in response to high-fat diets. The report explains how a high-fat diet reduces the thickness of the mucous layer, making it easier for bacteria to disrupt the tight junction proteins and increase intestinal permeability, thus leading to inflammation and potential IBD. Research on mice models confirms that a high-fat diet impairs epithelial barrier function, leading to reduced expression of tight junction proteins and increased susceptibility to inflammation. The conclusion emphasizes the negative impact of obesity on intestinal barrier function, resulting in increased inflammatory processes and a direct link to IBD through metabolic changes.

Running Head: OBESITY
Obesity
Name of the Student
Name of the University
Author Note

OBESITY
Introduction
The paper deals with the effect of obesity on intestinal barrier function. Further, the
relation of obesity to IBD is explained.
Effect of obesity on intestinal barrier function
Obesity is associated with metabolic alterations in the body such as insulin resistance and
glucose intolerance. Metabolic syndrome manifest as low-grade systemic inflammation and is
directly associated with the intestinal barriers dysfunction. Inflammation is caused by the
lipopolysaccharide or LPS derived from the gut microbiota. This factor is associated with the
metabolic disease linked to obesity. LPS is the major component of bacterial cell wall (gram
negative bacteria). These bacteria can induce inflammation. Intestinal epithelium acts as barrier
in normal physiological conditions and inhibits the LPS translocation (Walters et al. 2014).
People with obesity consume high fat diet. The barrier function is changed by the high fat diet
due to reducing thickness of mucous layer. Thus, it is easy for the microbes to destroy the tight
junction protein and destroy the intestinal permeability. Poor permeability allows greater access
of bacteria to intestinal route. It consequently increases the inflammatory process resulting in
intestinal tissue injury wall. It results in inflammatory bowel disease or IBD (Seminerio et al.
2015). Thus, obesity is associated with IBD. Several experiments conducted with mice model
showed manifestation of inflammatory bowel disease showed clear defect in epithelial barrier
defects. In mice models, epithelial tight junction proteins were poorly expressed when kept on
high fat diet (König et al. 2016).

OBESITY
Conclusion
In conclusion obesity negatively impacts the intestinal barrier function leading to
increases in inflammatory process initiated by bacteria. This barrier injury is manifest as IBD.
Hence, obesity is related to IBD via metabolic alterations.

OBESITY
References
König, J., Wells, J., Cani, P.D., García-Ródenas, C.L., MacDonald, T., Mercenier, A., Whyte, J.,
Troost, F. and Brummer, R.J., 2016. Human intestinal barrier function in health and
disease. Clinical and translational gastroenterology, 7(10), p.e196.
Seminerio, J.L., Koutroubakis, I.E., Ramos-Rivers, C., Hashash, J.G., Dudekula, A., Regueiro,
M., Baidoo, L., Barrie, A., Swoger, J., Schwartz, M. and Weyant, K., 2015. Impact of obesity on
the management and clinical course of patients with inflammatory bowel disease. Inflammatory
bowel diseases, 21(12), pp.2857-2863.
Walters, W.A., Xu, Z. and Knight, R., 2014. Meta‐analyses of human gut microbes associated
with obesity and IBD. FEBS letters, 588(22), pp.4223-4233.