Deletion of the protein Ecscr enhances insulin sensitivity and protects mice on a high fat diet from obesity reports a paper published in Nature Communications. The work suggests that inactivation of this protein may have therapeutic potential for the control of type-2 diabetes and obesity related metabolic disorders.
Insulin resistance is closely associated with obesity and is one of the earliest symptoms of type-2 diabetes. Endothelial cells (ECs) are known to be involved in the development of insulin resistance and Koji Ikeda and colleagues now show that deletion of Ecscr, a transmembrane protein that regulates EC signalling, protects mice on a high fat diet from obesity and obesity related metabolic disorders. They demonstrate that Ecscr-deficient mice fed a normal diet show improved glucose tolerance and enhanced insulin sensitivity. This is without changes in body weight and body fat mass. The team then reversed the method and noted that activating Ecscr impairs insulin sensitivity and predisposes the mice to obesity.
This work sheds light on EC-mediated regulation of systemic energy metabolism and glucose homeostasis and could represent a new therapy for treating metabolic syndrome.
Environment: Value of national parks’ impact on mental health estimatedNature Communications
Nature Reviews Endocrinology: A new approach for assessing health risks of endocrine disruptorsNature Reviews Endocrinology
Neuroscience: A brain-scanning bike helmetNature Communications