| Grant number: | 17/18498-6 |
| Support Opportunities: | Regular Research Grants |
| Start date: | August 01, 2018 |
| End date: | July 31, 2020 |
| Field of knowledge: | Health Sciences - Nutrition - Nutrition Biochemistry |
| Principal Investigator: | Patrícia de Oliveira Prada |
| Grantee: | Patrícia de Oliveira Prada |
| Host Institution: | Faculdade de Ciências Aplicadas (FCA). Universidade Estadual de Campinas (UNICAMP). Limeira , SP, Brazil |
Abstract
Exposure to air pollution has been highlighted as an important risk factor for morbidity and mortality in the world. Several pollutants, such as particulate matter weighing d 2.5 ¼m (MP2.5), as well as one of its chemical compounds, 1,2-naphthoquinone (1,2-NQ), obtained by burning diesel, have been associated with the genesis of chronic diseases, including type 2 diabetes mellitus (T2D). It is known that the perinatal environment has a permanent impact on the formation of tissue structure and metabolism. However, it has not yet been demonstrated by, which molecular and epigenetic mechanisms, early exposure to pollutants, could be determinant for the genesis of obesity and T2D. Thus, the aims of the present study are to investigate: 1) changes in body weight, body composition (DEXA), food intake, energy expenditure (CLAMS), fasting glycemia, insulinemia, leptinemia, glucose and insulin tolerance, pyruvate tolerance. In addition, to evaluate by flow cytometry the serum and adipose levels of cytokines, the number and phenotype of macrophages in the epididymal adipose tissue and in the washed peritoneal cavity; 2) the anorexigenic effect and intracellular signaling in the hypothalamus in response to leptin and insulin in the offspring (8 and 15 weeks of age) whose mothers will be exposed to 1,2-NQ or MP2,5 or filtrated air (FA) during the perinatal period. If changes in the anorectic response to these hormones are observed, the protein expression of SOCS-3, PTP1B and TCPTP will be investigated in the hypothalamus of the offspring as possible mechanisms of resistance to these hormones; As aim 3) to investigate the DNA methylation levels, histone and gene expression modification of NPY (neuropeptide Y), AgRP (agouti-related-protein), POMC (proopimelanocortin), TRH and CRHR1 (corticotrophin releasing hormone receptor 1) in the hypothalamus; Prmd16 (PR domain containing 16) and UCP1 (uncoupling protein 1) in white and brown adipose tissue and Pdx1 (pancreatic and duodenal homeobox 1), insulin and Ngn3 (neurogenin 3) in the pancreas of the offspring (8 weeks of age) whose mothers were exposed to 1,2-NQ or MP2.5 or FA during the perinatal period. Finally, the aim 4) to investigate the DNA methylation levels, histone gene expression modification in the serum of females (exposed and non-exposed) before and after gestation for future comparison with the profile of the pups. (AU)
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