Location: Location not imported yet.Title: Leptin and reproductive function) Author
Submitted to: Biochimie
Publication Type: Review article
Publication Acceptance Date: 2/17/2011
Publication Date: 3/2/2012
Citation: Hausman, G.J., Barb, C.R., Lents, C.A. 2012. Leptin and reproductive function. Biochimie. 94:2075-2081. Interpretive Summary: Leptin is an important metabolic signal made and secreted by fat cells. Leptin monitors the amount of body fat, nutritional status and shifts in the regulators of the reproductive system. A new neural regulator called kisspeptin is a key part of the central pathway by which leptin affects secretion of ket regulators of reproduction. Infertility observed in animals with alterations in circulating levels of leptin or alterations in brain sensitivity to leptin can partially be explained by suppression of kisspeptin. Continued examination for new neural regulators will ultimately result in the capability to control reproduction through the leptin system.
Technical Abstract: Adipose tissue plays a dynamic role in whole-body homeostasis by acting as an endocrine organ. Collective evidence indicates a strong link between neural influences and adipocyte expression and secretion of leptin. Developmental changes in these relationships are considered important for pubertal transition in reproductive function. Leptin augments secretion of gonadotropin hormones, which are essential for initiation and maintenance of normal reproductive function, by acting centrally at the hypothalamus to regulate the gonadotropin-releasing hormone (GnRH) neuronal activity. The effects of leptin on GnRH are mediated through interneuronal pathways involving neuropeptide-Y, proopiomelanocortin and kisspeptin. Increased infertility associated with diet induced obesity or central leptin resistance are likely mediated through the kisspeptin-GnRH pathway. Leptin further regulates reproductive function by altering the sensitivity of the pituitary gland to GnRH and acting at the ovary to regulate follicular and luteal steroidogenesis.