Characterization of rapid POMC regulation mechanisms involved in high-fat diet response

• Grant number: 14/00742-0
• Support Opportunities: Scholarships in Brazil - Post-Doctoral
• Effective date (Start): August 01, 2014
• Effective date (End): May 31, 2018
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Licio Augusto Velloso
• Grantee: Daniela Soares Razolli
• Host Institution: Faculdade de Ciências Médicas (FCM). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
• Associated research grant: 13/07607-8 - OCRC - Obesity and Comorbidities Research Center, AP.CEPID
• Associated scholarship(s): 16/23271-8 - Characterization of mechanisms involved on early regulation of POMC neurons in response to saturated fatty acids, BE.EP.PD

Abstract

Obesity is characterized by genetic, metabolic, hormonal and environment factors association. It is a major risk factor for insulin resistance, cardiovascular diseases, hypertension, dyslipidemia and certain types of cancer, impacting in life quality and mortality rates. Obesity provides public health elevated costs and affects more than 500 million humans worldwide, considered one of the most clinical-epidemiological phenomenons in the world. Studies developed in the past ten years showed that saturated fat acids acting through specific receptors trigger inflammatory cell signaling involved with inflammatory mediators, endoplasmatic reticulum stress and apoptosis of hypothalamic neurons that control food intake and termogenesis. It impairs gut-brain signaling and gastrointestinal peptides secretion. High-fat diet consume promotes hypothalamic inflammation and impairs leptin and insulin anorexigenc effects, resulting in weight gain. Our lab recently showed that hypothalamic neurons signaling disruption in obese propone mice occur in the early periods after high-fat diet consumption. This data suggests that neural circuit disruption appears before weight gain and chronic inflammation. Therefore, the mechanisms responsible for early hypothamalic neuronal disruption are still unknown. This project aims to identify the mechanisms involved with this energetic homeostasis disruption. (AU)