Endocrine Abstracts

The G protein-coupled receptor (GPCR) kinase 2, GRK2, is a ubiquitous serine/threonine protein kinase that is able to phosphorylate and desensitize the active form of several GPCR. Compelling, as yet limited, evidence from in vitro studies have suggested a potential role of GRK2 in mediating desensitization of Gpr54, the canonical receptor for kisspeptins that is abundantly expressed in GnRH neurons. Yet, although kisspeptins have been universally recognized as essent...

Obesity and its comorbidities are reaching epidemic proportions. Maternal obesity is known to predispose the offspring to metabolic disorders, independently of genetic inheritance. This intergenerational transmission has also been suggested for paternal obesity during the pre-conception stage, as it appears to have a negative impact on the metabolic and reproductive health of the offspring, likely via epigenetic changes in spermatozoa. However, whether paternal obesity sensiti...

While female fertility is known to be sensitive to conditions of low body fuel reserves, the reproductive consequences of persistent energy excess remain ill defined. Yet, the pandemic proportions of obesity, and its potential impact on the gonadotropic axis, call for a better understanding of this phenomenon. Alike, the influence of ovarian hormones on the pathophysiology of obesity and its complications merits further investigation. In this work, we aimed to elucidate the me...

Childhood obesity has become a major health problem, which is coupled to different adverse outcomes and diseases. The escalating prevalence of child obesity parallels that of alterations in pubertal timing, also linked to higher disease burden later on life. Yet, the mechanisms underlying for this association remain unfolded. Ceramides, ubiquitous signaling molecules involved in numerous biological processes, have emerged as mediators of metabolic disorders and transmitters fo...

Mkrn3, the maternally imprinted gene encoding the makorin RING-finger protein-3, has recently emerged as putative pubertal repressor, as evidenced by central precocity caused by MKRN3 mutations in humans; yet, the molecular underpinnings of this key regulatory action remain largely unexplored. We report herein that the microRNA, miR-30, with three binding sites in a highly conserved region of its 3’-untranslated region (UTR), operates as repressor of Mkrn3 to control pube...