| Grant number: | 13/07908-8 |
| Support Opportunities: | Regular Research Grants |
| Start date: | July 01, 2015 |
| End date: | June 30, 2017 |
| Field of knowledge: | Biological Sciences - Physiology |
| Principal Investigator: | Renata Frazão |
| Grantee: | Renata Frazão |
| Host Institution: | Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil |
| Associated researchers: | Jose Donato Junior |
Abstract
The average age in which children have shown indicators of the onset of puberty, such as the thelarche or menarche, has declined over the decades. This fact is alarming because early puberty brings several negative implications. For example, early exposure to sex hormones increases the risk for developing cancers in reproductive organs. The early onset of puberty increases the incidence of social offenses in adolescence and can lead to psychosocial problems, when the child has not yet reached a cognitive age which is appropriate to deal with the changes that happen to your own body. In addition, the anticipation of puberty promotes precocious sexual initiation, increases the number of pregnant adolescents and can affect somatic growth. There are some hypotheses that try to explain the early onset of puberty today, but a well-known fact is that a large proportion of children are overweight. The excess of the body fat changes leptin circulating levels and the responsiveness to this hormone in the hypothalamus (leptin resistance). These changes, in turn, may contribute to an earlier onset of puberty. Therefore, this project aims to investigate the responsible mechanisms for inducing early onset of puberty in overweight children, with emphasis on the possible role played by the hormone leptin. We propose experiments aimed at manipulating circulating leptin levels and/or the sensitivity to this hormone through tissue-specific inactivation of Socs3 gene or in mouse models of childhood obesity. Thus, we will evaluate the progression of sexual maturation in these mice, correlating these data with information on leptin sensitivity, metabolic cues (body weight and leptin levels) and neuronal activity. In addition, we will study possible changes in the acute response to the effects induced by leptin in different sexual maturation stages in hypothalamic nuclei potentially involved in the control of puberty. Based on these data, we will perform molecular analyzes in these nuclei to identify potential genes that may explain the effects of leptin on the onset of puberty. In summary, this project has the potential to improve our understanding about the molecular mechanisms responsible for the precocious puberty nowadays. (AU)
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