Endocrine Abstracts

Excessive glucocorticoid action is detrimental to metabolic health. The last 15 years has seen the emergence of enzymatic intra-cellular glucocorticoid reactivation, driven by the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), as a key mechanism contributing to glucocorticoid action. In most contexts, high intracellular glucocorticoid regeneration results in adverse metabolic effects. Inhibition or gene knockout of 11β-HSD1 is metabolically protectiv...

High systemic cortisol levels contribute to insulin resistance and may exacerbate the development of diabetes by impairing the insulin secretory response of the pancreatic beta-cells (β-cells). 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) is a key modulator of glucocorticoid effect within target tissues and high adipose or liver levels of this enzyme may contribute to obesity and/or metabolic disease. We investigated cellular localization of 11β-HSD1 ...

Advances in genetic approaches to bone physiology have expanded our understanding of the mechanisms by which bone and energy homeostasis interact. PHOSPHO1, a bone specific phosphatase is essential for the initiation of bone mineralisation. Here we now show that Phospho1 ablation confers a remarkable protection against obesity and diabetes in mice. To understand the mechanism whereby Phospho1 impacts metabolism, microarray analysis of osteoblasts, the primary...