ABSTRACT
Almost 50 years ago the obese mouse model was identified, and parabiosis studies were
able to demonstrate that some humoral factor was involved in adiposity, so that the
genetics and endocrine nature of this process have been apparent for many years. With
the discovery of leptin just a few years ago, early studies validated the role of
this protein product of the obese gene. Early studies in the obese mouse model (ob/ob mouse) demonstrated that the genetic basis was truly a deficiency in leptin. Coincidentally,
the relationship to fertility was also associated with leptin. These early studies
were also able to demonstrate a relationship to puberty and the time of pubertal development.
Very quickly, the recognition that the placenta was a source of leptin and that leptin
levels were elevated in pregnancy in a number of species also broadened our appreciation
of the relationship to reproductive functions. These many rapidly elucidated relationships
to leptin were reported soon after the identification and availability of leptin as
a research reagent and have firmly put leptin into the area of reproductive physiology
in addition to establishing roles in metabolism, satiety, and energy metabolism. Subsequent
studies have expanded all of these situations. Species beyond the rodent model, including
the human, have now introduced these physiologic studies into the clinical arena and
the role of leptin in fertility, puberty, pregnancy, and genetics. In this issue,
all of these topics are reviewed to bring the reader up to date with leptin and its
role in reproductive function, many of which overlap with the control of obesity.
KEYWORDS
Leptin - puberty - pregnancy - fertility - gender
