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Carol Elias

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Primary Appointment: Molec & Integrative Physiology
Primary PIBS Dept.: Molecular and Integrative Physiology
Other PIBS Depts.: Neuroscience
PubMed Name: Elias CF
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  Research in our laboratory is focused on determining the neural and molecular basis of the adipocyte-derived hormone leptin action in reproductive control. Humans and mice with loss-of-function mutations in leptin or leptin receptor genes are obese, diabetic and infertile. Leptin administration to leptin-deficient subjects (but not weight loss alone) restores their reproductive function and, therefore, leptin is thought to play a key role as metabolic signal to the reproductive axis. The link between metabolism and reproduction has been known for decades. It is well established that a minimum amount of stored energy is required to maintain the tone of the reproductive system. This concept is based on the idea that when survival is threatened by scarcity of food or increased energy demands, male and female of most species divert energy away from reproduction. This includes sexual maturation, the production of reproductive hormones and gametes, and the maintenance of pregnancy and lactation. If excessive leanness occurs in young women, puberty is often delayed. On the other side of the spectrum, excess stored energy also negatively impacts fertility. Obesity aggravates polycystic ovarian syndrome, ovulatory dysfunctions and may induce hypothalamic hypogonadism. In men, increased adiposity is a recognized factor for infertility likely due to defective gonadal steroidogenesis. In addition, more recently, studies have proposed a link between the obesity epidemics and the increasing rates of advance in puberty onset in girls. Taken together, these findings demonstrate that changing levels of key metabolic cues (e.g., leptin, insulin, ghrelin) are intrinsic components of pubertal maturation and the reproductive health. In our laboratory, we use a series of genetically modified mouse models, systems neuroscience and molecular tools to gain knowledge on the neuronal circuitry and molecular pathways linking leptin action in reproduction. We aim at determining the mechanisms by which metabolic imbalance disrupts the reproductive neuroendocrine axis.