Zinc in Gut-Brain Interaction in Autism and Neurological Disorders

Figure 1

Influence of zinc levels on gut formation. Zinc levels mediate villus height and villus/crypt ratio in the jejunum. Zinc deficiency results in a shortening and narrowing of the villi and thus a reduction in absorptive surface. This may be mediated by a reduction in mucosal cell proliferation and slower cell migration, as well as an increase in the number of apoptotic cells in villi and crypts. The zinc finger transcription factors Gata4 and Gata6 are involved in intestinal epithelial cell differentiation and promote enteroendocrine cell differentiation. Moreover, the number of goblet cells increases after zinc supplementation and is dependent on the activity of the zinc binding matrix metalloproteinase-9 (MMP-9). Goblet cells secrete mucins and an altered composition of intestinal mucin was reported in zinc deficient animals. Additionally, several alterations in the activities of brush border enzymes result from zinc deficiency. The development of paneth cells is accelerated by the zinc dependent transcription repressor BLIMP1. Furthermore, zinc deficiency is accompanied with mucosal necrosis and ulceration, inflammation, and oedema.