Certain defects in the way the mitochondria work may lead to diabetes, and the ways our bodies adapt to high blood sugars share many features with the ways our bodies respond to mitochondrial disease.
Children’s Hospital researchers recently identified a network of signaling molecules that acts like a “fuse box,” regulating the effects of defective energy flow in mitochondrial respiratory chain diseases — a set of difficult-to-treat genetic-based energy disorders. Using that knowledge, they showed that a form of vitamin B3 partially restores normal functioning in cells taken from patients with mitochondrial disease.
The Roizen Lab aims to understand non-calciometabolic vitamin D effects and to use this understanding to design new therapies for common diseases like sarcopenia and obesity.
