“Lethal milk”

Zinc deficiency is sometimes diagnosed in infants who are exclusively breast-fed. It can occur because of a dysfunctional zinc transporter in the mother, which prevents zinc from being secreted into the breast milk through a special zinc transporter in the epithelial cells of the mammary gland (Chowanadisai et al., 2006). It could also be inherited.

Zinc is important for the production of lactose (milk sugar). In addition, infants with zinc deficiency may develop dermatitis on their face (image below), diarrhea, as well as neurological changes which may alter their behavior (Medscape).

A new study published in the American Journal of Physiology – Regulatory, Integrative and Comparative Physiology was designed to try to figure out what happens in animals that are missing the zinc transporter. These so-called “lethal milk” mice have a mutated version of the ZnT4 transporter resulting in low concentrations of zinc in their milk. Consuming milk devoid of zinc is lethal to neonatal mice, which is how the mutation gets its name. This study found that the mammary gland epithelial cells of the lethal milk mice accumulated fats, which means the cells are not able to secrete the lipids (and potentially other nutrients) into the milk as well as healthy mice. They also found the mutation caused the mice to have underdeveloped mammary glands with reduced milk volumes and a loss of milk production after only 2 days. Using this model, they hope to better understand how zinc deficiency develops in women with similar mutations in the ZnT4 gene.


W Chowanadisai, B Lönnerdal, SL Kelleher. Identification of a mutation in SLC30A2 (ZnT-2) in women with low milk zinc concentration that results in transient neonatal zinc deficiency. Journal of Biological Chemistry. 281: 39699-39707, 2006.

, , , ZnT4 (SLC30A4)-null (“lethal milk”) mice have defects in mammary gland secretion and hallmarks of precocious involution during lactation. American Journal of Physiology – Regulatory, Integrative and Comparative Physiology. In Press.