Endocrine Abstracts

GnRH neurons are vital for reproductive competence. These neurons originate mainly in the nasal epithelium and migrate to the preoptic region of the hypothalamus during foetal development. Defective migration may result in Hypogonadotropic Hypogonadism (HH), a condition in which puberty is never or only partially achieved.Little is known about the molecular ontogeny and regulation of GnRH neurons. Their anatomical localisation and small numbers (about 10...

The gonadotropic hormones, LH and FSH are critical regulators of normal sexual functions including steroidogenesis and gametogenesis. Their essential role is underscored by the development of various hypogonadal phenotypes arising from genetic mutations. Constitutive activation of their cognate receptors also disturbs their function. We earlier showed that transgenic expression of an activating mouse Fshr mutant (mFSHRD580H) in granulosa c...

Gonadotropin-releasing hormone (GnRH) analogues are now the standard hormonal treatment for prostate cancer. A fundamental difference between GnRH agonist and antagonist treatment is the permanent suppression of both gonadotropins (LH and FSH) by antagonist, while a rebound in FSH is associated with agonist treatment. The benefits of antagonist include the immediate onset of action and profound long-term suppression of FSH, suggested to be an independent growth factor in prost...

Background: Self-limited delayed puberty (DP) often segregates in an autosomal dominant pattern, suggesting that inheritance is conferred by a small number of genes. However, the underlying genetic background is mostly unknown. By comparison, many genes have been identified where loss-of-function mutations lead to hypogonadotropic hypogonadism (HH). Despite likely overlap between the pathophysiology of delayed puberty and conditions of GnRH deficiency, few studies have examine...

PGC1 and RIP140 are key regulators of nuclear receptor signalling that control metabolic gene expression in adipose tissue, liver and muscle. PGC1 promotes whereas RIP140 represses the expression of a network of catabolic genes in adipose and muscle. Thus mice devoid of RIP140 accumulate less fat in adipose tissue and liver while mitochondrial biogenesis and respiration is increased in type 2 muscle fibres; as a consequence, the mice maintain their insulin sensitivity as they ...