Kisspeptin neurons are found in the hypothalamus and are critical for fertility through stimulation of gonadotropin-releasing hormone (GnRH) neurons. In addition to key roles in puberty onset, kisspeptin neurons govern underlying mechanism for sex steroid positive- and negative-feedback, and it is now commonly accepted – at least in rodents – that the ARC kisspeptin neurons act as the GnRH pulse generator. Moreover, kisspeptin neurons are now recognized as a central pathway responsible for conveying key homeostatic information to GnRH neurons to modulate fertility. Thus, in states of severely altered energy balance (either negative or positive) fertility is compromised, as is kisspeptin gene (Kiss1) expression in the arcuate nucleus. Furthermore, in addition to being expressed in GnRH neurons, the kisspeptin receptor (Kiss1r) is also expressed in other areas of the brain, as well as in the periphery, suggesting kisspeptin may have additional functions outside of governing reproductive status. Evidence is building for a direct role for kisspeptin in regulating energy balance and metabolism. Interestingly, kisspeptin neurons located in the arcuate nucleus are anatomically linked to anorexigenic POMC neurons and orexigenic NPY neurons. Thus, kisspeptin may have a role in energy balance and our observations indicated that Kiss1r knockout mice displayed late onset obesity and reduced energy expenditure. Moreover, recent data suggest that this obesity may be primarily due to altered uncoupling protein-1 (UCP1) mRNA expression in brown adipose tissue (BAT). Kisspeptin receptor is expressed in BAT, but its role there does not appear to be consistent with the obesity in Kiss1r knockout mice. Overall, in addition to regulating reproduction, kisspeptin signaling may also be an important regulator of metabolism and adiposity but the precise mechanistic pathways are yet to be determined.