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Abstract
Leptin, a 16-KD protein secreted primarily by adipose tissue, was first discovered
in the search for a satiety signal. When administered into the brain, leptin depresses
appetite. Interestingly, hyperphagic, obese, transgenic mice with leptin deficiency
were noted to be reproductively incompetent, and administration of leptin restored
their fertility. These pivotal observations led to numerous studies on the site of
action of leptin within the hypothalamo-hypophyseal-gonadal axis, and a variety of
models have been used ranging from the prepubertal condition to fasting suppression
of reproductive hormones. The preponderance of studies thus far has focused on how
leptin serves as a metabolic signal of energy balance within the neuroendocrine system,
particularly as a regulator of GnRH/LH secretion. Less research has been conducted
with other components of the reproductive system, but local effects of leptin have
been demonstrated in the gonads where hyperleptinemia suppresses steroidogenesis and
potentially affects gamete maturation. This presentation will review the major concepts
for the role of leptin in the modulation of fertility and will consider the potential
use of leptin in assisted reproductive technology and embryo transfer.