Endocrine Abstracts

Although primary aldosteronism (PA) is considered to be the most prevalent cause of secondary hypertension the underlying genetic mechanisms have been elucidated only for the rare familial forms of the disease. In an attempt to define novel genetic loci involved in the pathophysiology of PA a phenotype-driven mutagenesis screening after treatment with the alkylating agent N-ethyl-N-nitrosourea was established for the parameter aldosterone. The aldosterone values ...

White adipose tissue acts as an endocrine organ that secretes a variety of adipokines and coordinates a number of biological processes such as energy homeostasis, neuroendocrine and immune functions. Recent studies demonstrated that abundant adipose tissue depots (particularly visceral adipose tissue), by producing inflammatory cytokines, contribute to chronic low-grade inflammation processes which may underlie the pathogenesis of metabolic disorders such as obesity, atheroscl...

By a systematic approach we investigated the interaction of a selective number of GPCRs that are expressed in the arcuate nucleus and known to play an essential role in hypothalamic weight regulation. Based on the results of a sandwich ELISA and fluorescence resonance energy transfer (FRET) approach we report the interaction of the melanocortin three receptor (MC3R) and the growth hormone secretagogue receptor (GHSR) which are coexpressed on arcuate NPY/AgRP neurons. Fu...

The Src substrate associated in mitosis of 68 kDa (Sam68) is a KH-type RNA binding protein that has been shown to regulate several aspects of RNA metabolism. The tyrosine phosphorylation of Sam68 was shown to negatively regulate its RNA binding activity and hence it was termed a Signal Transduction Activator of RNA (STAR) protein. Although KH-type RNA binding domains are known to mediate specific protein-RNA interactions, their RNA targets remain elusive. Nevertheless, Sam68 h...

Objectives: Male pseudohermaphroditism, or Leydig cell hypoplasia (LCH), is an autosomal recessive disorder in individuals with a 46, XY karyotype, characterized by a predominantly female phenotype despite the presence of testicular structures. It is caused by mutations in the luteinizing hormone/chorionic gonadotropin receptor gene (LHCGR), which impair either LH/CG binding or signal transduction. However, molecular analysis has revealed that the LHCGR is apparently normal in...