Abstract Zinc deficiency is a global health problem affecting approximately one billion people and is associated with serious health consequences, including impaired immune function and an increased susceptibility to infections and inflammation 1,2. It is also linked to disrupted intestinal homeostasis and a higher incidence of diarrheal diseases 1,3. In addition to the severe degeneration of the intestinal epithelium observed during zinc deficiency 4, the mucus barrier in the intestinal tract is also disrupted 5,6. Intestinal mucus does not only protect the underlying epithelium and provides a habitat for the commensal microbiota 7, it also plays a critical role in the absorption of trace elements such as zinc 8,9. Our previous studies conducted using the human goblet cell model HT29‐MTX already indicated that zinc deficiency alters the intestinal O ‐glycome, as the gene expression of several mucins and glycosyltransferases (GTFs) was dysregulated and the O ‐glycosylation pattern of mucins secreted by the cells were changed, with a significant increase of shorter glycans 6. However, the consequences of these observations for the entire mucin O ‐glycome remain to be fully investigated.
Schüßler et al. (2026) studied this question.