On June 13, Bernal-Mizrachi Lab had their article titled “Embryonic vitamin D deficiency programs hematopoietic stem cells to induce type 2 diabetes,” published by Springer Nature.
Currently, the risk of later-in-life type 2 diabetes from embryonic immune cell programming is unknown. It is possible that environmental factors can cause metabolic disease by altering the fetal genome.
In their research, the authors utilized mouse models to demonstrate and assess the implications of vitamin D deficiency on insulin. Stating that “transplantation of fetal hematopoietic stem cells (HSCs) made vitamin D deficient in utero induced diabetes in vitamin D-sufficient mice.” In comparison of the models to human cord blood, they found similarities in expression changes and secretion, resulting in adipocyte insulin resistance.
In summary, their findings suggest that “vitamin D deficiency during embryonic development has epigenetic consequences impacting the systemic metabolic milieu;” thus, inducing type 2 diabetes.
Oh J, Riek AE, Bauerle KT, Dusso A, McNerney KP, Barve RA, Darwech I, Sprague JE, Moynihan C, Zhang RM, Kutz G, Wang T, Xing X, Li D, Mrad M, Wigge NM, Castelblanco E, Collin A, Bambouskova M, Head RD, Sands MS, Bernal-Mizrachi C. Embryonic vitamin D deficiency programs hematopoietic stem cells to induce type 2 diabetes. Nat Commun. 2023 Jun 13;14(1):3278. doi: 10.1038/s41467-023-38849-z. PMID: 37311757; PMCID: PMC10264405.