Talk Title: "Exploiting the Genomic Mechanism of Renal Vitamin D Metabolism to Understand the Consequences of Supplementation on Non-Renal Calcitriol Production"

The Meyer lab studies the dynamic chromatin environment responsible for serum calcium and phosphate maintenance and the impacts of vitamin D metabolism in skeletal, renal, and intestinal biology. A triumvirate of endocrine hormones – parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), and calcitriol (1,25(OH)2D3) – maintain this delicate balance by influencing enzymes, transporters, and transcription factors to drive genomic change. When dysfunctional, these mechanisms allow chronic inflammation and disease progression to worsen in chronic kidney disease-metabolic bone disorder (CKD-MBD), atherosclerosis, inflammatory bowel disease (IBD), and many others. Low vitamin D status has a correlation with an increase in cancer risk in cancers such as colorectal, breast, and prostate. Higher vitamin D status has been linked to longer survival rates in cancer patients. Additionally, vitamin D deficiency is associated with low birth weight, small size for gestational age, and the increased susceptibility to obesity, insulin resistance, and diabetes later in life. Recently, maternal vitamin D deficiency in mice was found to imprint an epigenetic program in immune cells leading to insulin resistance and diabetes in offspring later in life. Dietary and nutritional supplementation of vitamin D rapidly corrects the body’s mineral deficiencies, however its ability to ameliorate inflammatory disease progression or improve cancer outcomes remains controversial. We study the intricate genomic and molecular mechanisms that regulate the biological changes controlling the intersection of metabolism, inflammation, and disease progression using unique animal models, genomic editing techniques, and -omics bioinformatic approaches to generate unbiased interrogation of chromatin changes.