title: An updated view of leptin on implantation and pregnancy: a review.
abstract: The hormone leptin, which is thought to be primarily produced by adipose tissue, is a polypeptide that was initially characterized by its ability to regulate food intake and energy metabolism. Leptin appears to signal the status of body energy stores to the brain, resulting in the regulation of food intake and whole-body energy expenditure. Subsequently, it was recognized as a cytokine with a wide range of peripheral actions and is involved in the regulation of a number of physiological systems including reproduction. In the fed state, leptin circulates in the plasma in proportion to body adiposity in all species studied to date. However other factors such as sex, age, body mass index (BMI), sex steroids and pregnancy may also affect leptin levels in plasma. In pregnant mice and humans, the placenta is also a major site of leptin expression. Leptin circulates in biological fluids both as free protein and in a form that is bound to the soluble isoform of its receptor or other binding proteins such as one of the immunoglobulin superfamily members Siglec-6 (OB-BP1). Although the actions of leptin in the control of reproductive function are thought to be exerted mainly via the hypothalamic-pituitary-gonadal axis, there have also been reports of local direct effects of leptin at the peripheral level, however, these data appear contradictory. Therefore, there is a need to summarize the current status of research outcomes and analyze the possible reasons for differing results and thus provide researchers with new insight in designing experiments to investigate leptin effect on reproduction. Most importantly, our recent experimental data suggesting that reproductive performance is improved by decreasing concentrations of peripheral leptin was unexpected and cannot be explained by hypotheses drawn from the experiments of excessive exogenous leptin administration to normal animals or ob/ob mice.
authors.affiliation: University of New England, Armidale, Australia. jmcfarla@une.edu.au.
authors.forename: M
authors.initials: M
authors.lastname: Herrid
authors.forename: S K A
authors.initials: SK
authors.lastname: Palanisamy
authors.forename: U A
authors.initials: UA
authors.lastname: Ciller
authors.forename: R
authors.initials: R
authors.lastname: Fan
authors.forename: P
authors.initials: P
authors.lastname: Moens
authors.forename: N A
authors.initials: NA
authors.lastname: Smart
authors.forename: J R
authors.initials: JR
authors.lastname: McFarlane
mesh_terms: D000818:Animals; D010064:Embryo Implantation; D005260:Female; D005298:Fertility; D006801:Humans; D020738:Leptin / Q000378:metabolism*; D011247:Pregnancy; D012098:Reproduction; D015398:Signal Transduction
chemical_list: D020738:Leptin