Low manganese levels may worsen inflammatory bowel disease

Researchers at the University of Michigan have further studied the relationship between manganese deficiency and inflammatory bowel disease and found that low levels of this micronutrient can worsen intestinal damage and inflammation.

Their study, published in Nature Communicationsfocuses on the genetic variant of the manganese transporter SLC39A8, which affects manganese levels in the body. People with a genetic variant of SLC39A8, or ZIP8, may suffer from manganese deficiency, which this and previous studies have linked to inflammatory bowel diseases such as Crohn’s disease and colitis.

“Our research reveals the crucial role of the manganese transporter SLC39A8 in maintaining healthy manganese levels and gut health. Our work also opens new therapeutic possibilities for patients with IBD related to manganese imbalance,” said Young-Ah Seo, corresponding author of the study and associate professor of nutritional sciences in the UM School of Public Health.

Manganese is essential for many physiological functions in the body, including immune responses, bone formation, and carbohydrate metabolism. This mineral, which is present in the body and in foods and other minerals, is abundant in plant-based foods such as whole grains, legumes, rice, nuts, and vegetables. However, current animal-based diets (meat, fish, poultry, eggs, dairy) do not contain sufficient manganese.

The study cites evidence that dietary manganese consumption has declined by more than 40% over the past 15 years in developed countries, including the United States.

This decrease and deficiency are likely linked to an increase in intestinal disease, the researchers say, and this manganese deficiency may be responsible for weakening the epithelial barrier of the intestines, leading to disease.

The SLC39A8 gene is essential for the regulation of manganese levels, acting as a trigger for cellular uptake of zinc, iron, manganese, and cadmium. SLC39A8-related diseases have only recently been discovered, and the impact of the disease-associated SLC39A8 A391T variant on human health and disease is only beginning to be appreciated.