Researchers at the University of Michigan have uncovered new insights into how manganese deficiency may worsen inflammatory bowel disease (IBD). Their study, published in Nature Communications, explores the connection between low manganese levels and increased intestinal inflammation and damage.
The research focuses on the SLC39A8 gene, which encodes a manganese transporter known as ZIP8. Variations in this gene can lead to manganese deficiency. Previous studies have suggested a link between such deficiencies and inflammatory bowel conditions, including Crohn’s disease and ulcerative colitis.
Manganese is crucial for various bodily functions, such as immune system support, bone health, and carbohydrate metabolism. It is found in plant-based foods like whole grains, legumes, nuts, and vegetables. However, manganese is less abundant in animal-based diets, which include meat, fish, poultry, eggs, and dairy products.
The study highlights a significant decline in manganese intake in developed countries over the past 15 years, with a decrease of more than 40% in the United States. Researchers believe this reduction in manganese consumption may contribute to a rise in bowel diseases. They suggest that manganese deficiency could compromise the intestinal barrier, making it more susceptible to disease.
The SLC39A8 gene plays a vital role in managing manganese levels by regulating the uptake of manganese, zinc, iron, and cadmium into cells. The impact of the SLC39A8 A391T variant on health is still being studied, but it is becoming increasingly clear that this genetic variation affects disease susceptibility.
The study team includes Eun-Kyung Choi, Jin-Ho Park, and Luisa Aring from the U-M School of Public Health, along with Thekkelnaycke Rajendiran, Chithra Muraleedharan, Vicky Garcia-Hernandez, Nobuhiko Kamada, Asma Nusrat, Tanu Soni, Linda Samuelson, and Shigeki Iwase from the U-M Medical School.
