Methylation and gene expression patterns of inflammation and energetic metabolism in offspring of rats subjected to folic acid supplemented diet

• Grant number: 18/03291-0
• Support Opportunities: Regular Research Grants
• Duration: July 01, 2018 - March 31, 2021
• Field of knowledge: Health Sciences - Nutrition - Nutrition Biochemistry
• Principal Investigator: Helio Vannucchi
• Grantee: Helio Vannucchi
• Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
• Associated researchers: Carla Barbosa Nonino

Abstract

Epigenetics involves mechanisms that are essential for the proper embryonic development of mammals, and changes at this stage may lead to various metabolic disorders, such as obesity. This disease is characterized by chronic inflammation of low grade, which leads to numerous diseases that seriously compromise the health of the individual, in addition to having a multifactorial origin involving both environmental and genetic factors. Objective - To investigate the expression and methylation patterns of interleukin 6 (IL6), tumor necrosis factor alpha (TNF-alpha) and interleukin 1 beta (IL1b), sirtuin 1 (SIRT1), proliferator-activated receptor peroxisome alpha (PGC1-±), gamma peroxisome proliferator-activated receptor (PPAR-³) and forkhead Box 1 (FOXO1) in the offspring of rats submitted to deficient and folic acid supplemented diets. Methods - Wistar rats will be selected and two couples / treatment groups (control group, folic acid deficient group and folic acid supplemented group) will be formed for mating. Samples of adipose tissue (white and brown) and liver will be collected from which DNA, RNA and proteins will be extracted using specific commercial kits. With the said biological samples will be carried out analyzes of the methylation pattern (DNA), gene expression by real-time PCR (mRNA) and proteomics by Western blotting. The results of this study are expected to provide a better understanding of the molecular mechanisms related to fetal epigenetic reprogramming of inflammation and energetic metabolism genes involved with obesity and of adequate supply of folic acid during the embryonic / fetal development period. (AU)