Evaluation of the mitochondrial-associated membranes (MAM) integrity of pancreatic islets subjected to amino acid restriction in association with fatty acids

• Grant number: 20/02164-4
• Support Opportunities: Scholarships abroad - Research Internship - Doctorate
• Start date: November 30, 2021
• End date: November 29, 2022
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Everardo Magalhães Carneiro
• Grantee: Thiago dos Reis Araujo
• Supervisor: Rieusset Jennifer
• Host Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
• Institution abroad: Université Claude Bernard Lyon 1, France
• Associated to the scholarship: 17/24851-0 - In vitro and in vivo analysis of the mechanism of action of tauroursodeoxycholic acid (TUDCA) on the mitochondrial function of pancreatic islets and insulin-responsive tissues submitted to amino acid restriction in association with fatty acids, BP.DR

Abstract

Malnutrition is a metabolic disorder that affects about 795 million individuals around the globe, resulting from the reduction in energy or nutritional intake in a given phase of life. It is well known that nutritional deficiency during development and maturation generates disturbances in communication, biogenesis and mitochondrial function in different rodent and human tissues, leading to imbalance of glycemic control and rupture in energy homeostasis, predisposing to the development of obesity and type 2 diabetes (T2D) in adulthood. Data published by our research group demonstrated that protein malnourished mice exposure to hyperlipid diet in adulthood leads to reduced insulin secretion and mitochondrial density besides increasing production of reactive oxygen species in the pancreatic islets. However, even knowing that the association between endoplasmic reticulum and mitochondria, defined as mitochondria-associated membranes (MAMs), is important for maintaining pancreatic ² cell function, as well as for its survival, no work has characterized MAM integrity and mitochondrial metabolism in this experimental model. Therefore, with the development of this collaborative project, we will characterize the mitochondrial metabolism and MAM integrity in pancreatic islets in the malnutrition model associated with obesity and thus describe using cellular approaches what possible mechanisms involved in the alteration of insulin secretion observed in this model. (AU)