Autophagy involvment in the metabolic and inflammatory alterations in adipose tiss...
| Grant number: | 17/17403-1 |
| Support type: | Scholarships in Brazil - Scientific Initiation |
| Effective date (Start): | January 01, 2018 |
| Effective date (End): | June 30, 2020 |
| Field of knowledge: | Biological Sciences - Physiology - Physiology of Organs and Systems |
| Principal Investigator: | William Tadeu Lara Festuccia |
| Grantee: | Thayna dos Santos Vieira |
| Home Institution: | Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil |
| Associated research grant: | 15/19530-5 - Involvement of the nutrient sensor mTOR in the development of obesity associated chronic metabolic diseases, AP.TEM |
Abstract The exponential increase in obesity worldwide is an alarming problem as it increases the chances of developing other diseases associated with excessive adipose mass, such as Type II diabetes and insulin resistance. Currently in Brazil, about half of the population is overweight, progressing to a possible obesity. Therefore, a deeper understanding of the molecular mechanisms that determine adiposity is of major importance to develop new more effective strategies to treat obesity. In this sense, recent studies from our laboratory have shown that constitutive activation of mTOR complex 1 (mechanistic target of rapamycin, mTORC1) induced by the deletion of Tsc1 exclusively in adipocytes increases mitochondrial content and oxidative metabolism (oxygen consumption and fatty acid oxidation) in both visceral and subcutaneous fat, as well as, uncoupling protein 1 content in visceral fat. Herein, we will investigate how constitutive activation of mTORC1 promotes those phenotype. For this, we will test 2 hypotheses: 1) that the increase in mitochondrial content and oxidative metabolism induced by Tsc1 deletion result from the increased rates of protein synthesis in adipocytes induced by constitutive mTORC1 activation; 2) that the increased in visceral fat UCP1 content is mediated by an increase in transcriptional activities of PPAR±, PPARg, ER± or ERR±. (AU) | |