Endocrine Abstracts

Selenium (Se) represents an essential trace element and acts as catalytic entity in thyroid hormone deiodinases (Dio), glutathione peroxidases or thioredoxin reductases. Se-deficiencies worsen a variety of conditions of which some display a sex-bias, including certain forms of cancer, autoimmune- and infectious diseases. Using C57BI/6 mice as model organism, we determined enzymatic activities and transcript levels of certain selenoproteins in various tissues. mRNA levels of th...

An atypical form of resistance to thyroid hormone (RTH) leads to retarded growth and bone age in humans. Aberrant thyroid hormone levels (high T4, low T3, elevated rT3 and high/ normal TSH) indicate a defect in deiodinase-dependent thyroid hormone metabolism. Findings of reduced concentrations of plasma selenoproteins (SePP, GPx3) suggested a generalized defect of selenoprotein biosynthesis and led to the identification of mutations in the SECISBP2 gene. SECISBP2 is thought to...

Selenium (Se) is indispensable for enzymatic activities of glutathione peroxidases (GPx) involved in antioxidative defense and deiodinase isozymes (Dio) that control thyroid hormone (TH) action. Se deficiency can impact negatively on thyroid galnd funtioning and TH metabolism and thereby perturb development and metabolism. We have generated Se-deficient mice by genetic inactivation of Selenoprotein P (SePP), the main plasma Se carrier. SePP-KO mice display decreased serum and ...

Cathepsin K is a cysteine protease known for its importance in bone remodelling. Inhibitors of cathepsin K are in clinical trials for osteoporosis treatment, but side effects included altered levels of related cathepsins in peripheral organs and in the central nervous system (CNS). Importantly, cathepsin K has been identified not only in osteoclasts but also in most epithelia and, recently, in brain parenchyma. Lately, we have also shown that cathepsin K deficiency in mice ind...