Leptin and reproductive function

Adipose tissue plays a dynamic role in whole-body energy 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 gonadotropin-releasing hormone (GnRH) neuronal activity and secretion. 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. Furthermore, Leptin regulates reproductive function by altering the sensitivity of the pituitary gland to GnRH and acting at the ovary to regulate follicular and luteal steroidogenesis. Thus leptin serves as a putative signal that links metabolic status with the reproductive axis. The intent of this review is to examine the biological role of leptin with energy metabolism, and reproduction.

► Leptin alters secretion of gonadotropin hormones essential for normal reproduction. ► Leptin regulates hypothalamic gonadotropin-releasing hormone neuronal activity. ► Leptin affects on GnRH are mediated by NPY, proopiomelanocortin and kisspeptin. ► Kisspeptin-GnRH pathway mediates infertility due to obesity or leptin resistance. ► Adipose tissue leptin may be involved in leptin's influence on reproduction.