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.
News published in Agência FAPESP Newsletter about the scholarship: