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Evaluation of adipose tissue microRNA expression regulating neuro-adipose crosstalk in hyperlipidic diet induced obese mice offspring

Grant number: 16/08202-0
Support Opportunities:Scholarships in Brazil - Doctorate
Effective date (Start): August 01, 2016
Effective date (End): July 31, 2021
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Alice Cristina Rodrigues
Grantee:Erica de Sousa
Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Associated scholarship(s):18/13793-2 - The role of microRNA-22 in mice metabolic complications due to maternal obesity, BE.EP.DR


Obesity has been raised worldwide in an alarming way. It is broadly known that risk factors for obesity are a combination from genetics and environmental. In this context, from studies in animals and human we learned that epigenetics is an important risk factor, becoming clear that maternal metabolic status before and during pregnancy and lactation affects offspring metabolism for their whole lifetime. Among epigenetic mechanisms, microRNAs posttranscriptional regulation of gene expression in adipose tissue has been shown modified by diverse metabolic issues, like excessive weight gain and chronic cold exposure. On the other hand, communication between adipose tissue and nervous system regulates energy expenditure, and is also modified by obesity and cold exposure. However, there are no studies touching directly possible influence of maternal obesity on miRNAs modulating genes related to neuroadipose communication, although this field of research will probably bring highlights concerning metabolic programming. Since obesity is a transgenerational disorder, learning the effects of maternal obesity on offspring neuroadipose communication, which develops influenced by maternal metabolic status, means support future research for therapeutic approaches for obesity and comorbidities. Finally, the aim of this project is evaluating miRNAs expression modified by maternal obesity that can compromise neuroadipose communication, influencing offspring metabolism and capacity for adipose tissue browning.

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