Leptin and reproduction.

@article{Chehab2002LeptinAR,
  title={Leptin and reproduction.},
  author={Farid F. Chehab and Junyi Qiu and Khalid Mounzih and Amanda Ewart-Toland and Scott Ogus},
  journal={Nutrition reviews},
  year={2002},
  volume={60 10 Pt 2},
  pages={
          S39-46; discussion S68-84, 85-7
        }
}
Leptin, a hormone secreted from adipose tissue, plays an important role in reproductive physiology. It has been shown to stimulate the reproductive system by rescuing the sterility of leptin-deficient mice and advancing the onset of puberty in normal mice. Although leptin is not critical for the biology of pregnancy in mice, its ability to reduce food intake is blunted in mid-gestation suggesting that late pregnancy may be a leptin-resistant state. Modifier genes originating from the Balb/cJ… 
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Leptin and Female Reproductive Health
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This chapter illustrates the importance of leptin in female reproductive health, its role in the metabolic regulation of reproductive axis and its eventual pathophysiological implications in prevalent reproductive disorders.
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The aim of the present review is to study the role of leptin in carcinogenesis and its implications in cancer-related systemic inflammation.
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Does Genetic Variation in the Leptin Receptor Influence the Sympathetic Tone in Obesity?
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Emerging evidence supports a pathophysiological role for leptin in the hypertension associated with obesity because leptin resistance in the central nervous system appears selective.
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TLDR
The results demonstrate the importance of PI3K and melanocortin receptors in the transduction of leptin-induced renal sympathetic activation in obesity, and examine the role of phosphoinositol-3 kinase (PI3K) and melanoprotein receptors (MCR) in mediating the preserved renal SNA response to leptin in obesity.
Modulation of appetite by gonadal steroid hormones
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  • Biology, Medicine
    Philosophical Transactions of the Royal Society B: Biological Sciences
  • 2006
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A variety of peripheral feedback controls of eating, including ghrelin, cholecystokinin (CCK), glucagon, hepatic fatty acid oxidation, insulin and leptin, has been shown to be estradiol-sensitive under at least some conditions and may mediate the estrogenic inhibition of eating.
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It appears that a significant caloric perturbation is necessary for acute exercise to result in a significant reduction in leptin, and physical exercise and training have both inhibitory and stimulatory effects on leptin.
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References

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TLDR
Results suggest that leptin acts as a signal triggering puberty, thus supporting the hypothesis that fat accumulation enhances maturation of the reproductive tract.
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TLDR
It is proposed that leptin is the signal that informs the brain that energy stores are sufficient to support the high energy demands of reproduction, and may be a major determinant of the timing of puberty.
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TLDR
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TLDR
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TLDR
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TLDR
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TLDR
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