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ULK1/2 mediated autophagy: effects in hepatocyte energetic metabolism

Grant number: 18/13252-1
Support type:Scholarships abroad - Research Internship - Doctorate (Direct)
Effective date (Start): April 01, 2019
Effective date (End): March 31, 2020
Field of knowledge:Biological Sciences - Physiology
Principal Investigator:William Tadeu Lara Festuccia
Grantee:Milene Ortiz Silva
Supervisor abroad: Nicholas Ktistakis
Home Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Local de pesquisa : Babraham Institute, England  
Associated to the scholarship:17/12260-8 - Autophagy involvment in the metabolic and inflammatory alterations in adipose tissue associated with Obesity induced by high fat diet, BP.DD

Abstract

The central regulators of autophagy are the serine/threonine kinases unc-51 like autophagy activating kinase 1/2 (ULK1 and ULK2) that participate in the onset of the autophagic cellular process. These kinases in addition to initiate the autophagic cascade, seem to have interesting secondary roles in energy metabolism to coordinate the cellular response to starvation, such as increasing glycolysis flux, shunting carbon to the PPP pathway, producing NADPH, and controlling lipid metabolism in adipocytes or HCT116 cells. This proposal aims to investigate in Hep G2 cells (a model for hepatocytes) the metabolic effects of ULK1 and/or 2 that are dependent or independent of the autophagy machinery, such as fatty acid synthesis/lipolisys, glycogen accumulation/breakdown and glycolytic activity. Comprehending these kinases signaling may contribute greatly to therapeutic approaches for obesity, hepatic steatosis and aging.