ArticleScientific reports2026
Transcriptome, glycome, and mucinome analysis reveal zinc is essential for the composition of mucus in the human goblet cell model HT-29-MTX.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zinc (Zn) deficiency affects approximately 1 billion people worldwide with severe consequences for their health, including increased intestinal infections, inflammation, and diarrhea. Accordingly, the intestinal defense barrier is compromised, leading to epithelial destruction and alteration of mucus. However, the processes and the extent to which Zn deficiency affects mucin synthesis in intestinal goblet cells (GCs) remain poorly understood. To this end, we investigated the impact of Zn deficiency on mucin expression and glycosylation in the human GC model HT-29-MTX. Zn deprivation altered the GC transcriptome, affecting genes involved in Zn transport, mucin synthesis and glycosylation. Accordingly, mucus composition was changed in Zn-deficient GCs, significantly increasing MUC2 and MUC17 on the mRNA and protein level. Several Zn transporters, mostly those associated with the early secretory pathway (ESP), were dysregulated, indicating an adaptive response of cellular Zn homeostasis. Additionally, free Zn was markedly reduced in the ESP, a critical location for glycosylation. Zn deficit substantially changed mucin glycosylation, characterized by an increase in sialylation and a strong decrease in complex N-glycans. All these changes involved widespread dysregulation of glycosyltransferase expression, including an increase in COSMC, a Zn-binding chaperone essential for the core 1 O-glycan formation. Collectively, our in vitro findings demonstrate that Zn is a critical regulator of mucin production and glycosylation in GCs. Zn deficiency might weaken the protective and functional qualities of intestinal mucus, increasing the risk of infections and potentially disrupting host-microbiome interactions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.