Zinc supplementation as a bacterial diarrhea therapy in children

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Illustrations of bacterial diarrhea in children. (Source: Honest Docs)

Indonesia is one of the countries that have a high risk of zinc deficiency because more than 25% of the population suffer from zinc deficiency. The number is higher than the prevalence of zinc deficiency worldwide, which is 21%. WHO and UNICEF declared zinc as one of the therapies that must be administered to diarrhea to reduce the incidence of diarrhea for the next 2 – 3 months and prevent about 90% morbidity related to diarrhea in 2004.

Zinc is a component of many enzymes that are instrumental in the essential cellular function at all stages of the cell cycle. Zinc also acts as an antioxidant and also has a bactericidal effect. However, the mechanism of zinc to prevent deterioration of the function and structure of the intestines caused by lipopolysaccharides (LPS) produced by the Escherichia coli infection is still unclear. The purpose of this study is to investigate the effect of zinc against the destruction of intestinal integrity caused by the administration of LPS originating from E. coli.

The study was conducted on 32 Manly Wistar strain white rats with a weight of 80 grams with the age of 5 weeks and divided into two groups, i.e. standard zinc diet groups and zinc-deficient diet groups. Each of the groups is divided into two groups without zinc supplementation and groups with zinc supplementation. After the fifth week, the LPS is given on day 36 to induce the stress on the gastrointestinal tract that resembles diarrhea. The length of intestinal villi and the number of enterocytes in ileum tissue that evaluated in each of the experimental groups.

Epithelial damage resulting in a decrease of enterocytes number and a short of intestinal villi obtained in zinc deficiency groups in this study. Thus, zinc supplementation could repair the damage anatomically and functionally. Zinc deficiency will cause oxidative damage to the structural integrity of intestinal cell membranes so that it will alter the functioning of the cell membrane of the intestine.

Zinc supplementation administered in standard zinc groups can help retain the length of the villi and protect against anatomically damaged bowel damage. Under normal zinc conditions, zinc supplementation may increase endogenous zinc reserves and induce metallothionein synthesis in intestinal cells to provide anatomical protection against intestinal damage.

Lipopolysaccharides (LPS) impair the integrity of the intestine appears in the long decline of intestinal villi and the number of enterocytes in both zinc deficiency groups and standard zinc groups. There is an improvement in length of intestinal villi, and the number of enterocytes significantly gained after administration of zinc supplementation in both groups. The protective role of zinc on gastrointestinal diseases has been well known.

Zinc plays an essential role in maintaining the function and stability of intestinal membranes because zinc plays a role in the synthesis of RNA and DNA, so administering zinc supplementation will increase cell proliferation and protein synthesis. Zinc directly affects tissues with high growth rates, such as the gastrointestinal tract and immune system.

Previous studies also stated that zinc oxide had been shown to improve the function of the digestive tract by increasing mucosal thickness, high villi, and width of the small intestine. This research has shown that zinc supplementation will increase the length of intestinal villi and the number of enterocytes in rats with zinc deficiency and also in rats with standard zinc-exposed LPS. Zinc supplementation in rats with zinc deficiency (without exposure to LPS) also showed increased intestinal villi and the number of enterocytes. Furthermore, zinc plays an essential role in the gastrointestinal tract, a high growth rate network, in the synthesis of RNA and DNA that will be used for cellular proliferation and protein synthesis, especially on tissues with a high growth rate i.e. gastrointestinal tract. (*)

Author: Andy Darma

Details of the research available at


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