Embryonic vitamin D deficiency programs hematopoietic stem cells to induce type 2 diabetes

Embryonic vitamin D deficiency programs hematopoietic stem cells to induce type 2 diabetes

Blog Article

Abstract Environmental factors may alter the fetal genome to cause metabolic diseases.It is unknown whether embryonic immune cell programming impacts the risk of type 2 diabetes in later life.We demonstrate that transplantation of fetal hematopoietic stem cells (HSCs) made vitamin D deficient in utero induce diabetes in vitamin D-sufficient mice.

Vitamin D deficiency epigenetically iPhone X/XS suppresses Jarid2 expression and activates the Mef2/PGC1a pathway in HSCs, which persists in recipient bone marrow, resulting in adipose macrophage infiltration.These macrophages secrete miR106-5p, which promotes adipose insulin resistance by repressing PIK3 catalytic and regulatory subunits and down-regulating AKT signaling.Vitamin D-deficient monocytes from human cord blood have Laser and party lighting comparable Jarid2/Mef2/PGC1a expression changes and secrete miR-106b-5p, causing adipocyte insulin resistance.

These findings suggest that vitamin D deficiency during development has epigenetic consequences impacting the systemic metabolic milieu.