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Molecular mechanisms involved in pancreatic beta cell dysfunction and death in Diabetes Mellitus: strategies for the inhibition of these processes and restoration of the insular mass


Diabetes Mellitus is a chronic metabolic syndrome that affects hundreds of millions of people, and is the direct cause of death for over a million people every year. Severe chronic complications associated to it are the main cause of blindness and visual dysfunctions, limb amputation, kidney failure, neuropathies, and cardiovascular diseases. Maintaining glicemic homeostasis is crucial to avoid deaths and patient complications, including those related to other non-chronic diseases, such as Covid-19. The two main forms of the disease are type 1 Diabetes (DM1) that corresponds to 5-15%, and type 2 (DM2) that corresponds to 80-85% of all cases of Diabetes Mellitus. In DM2, the onset of the disease involves a genetic pre-disposition, associated with multiple environmental factors, being obesity one of the major factors that predispose the individual in developing this type of Diabetes. As for DM1, the pathogenesis is not yet fully understood, but it is known that the reduction of beta-cell mass occurs due the contact with cells from the immune system, associated with pro-inflammatory mediators such as the cytokines, leading to apoptosis. The reduction of insulin production and secretion, provoked by a progressive loss of function and mass of the beta cells, is a common characteristic for both DM1 and DM2. In this project, we will investigate interventions that could ameliorate DM, focusing on beta-cells, by studying molecular mechanisms that participate in their maturation, function, and mass, as well as in other tissues involved in the glicemic homeostasis regulation, such as skeletal muscle, liver, adipose tissue, and neural system. Also, we will focus on the participation of the vagus nerve and hypothalamic regulators in the energetic homeostasis of obese mouse and their actions upon the physiopathology of pancreatic islets. In addition, we will expand our investigation to isolated human islets, obtained from pancreas donated by patients, as well as in undifferentiated hPSC-beta cells (an area poorly developed in Brazil). Finally, we would like to state that our group possesses all the necessary structure and collaborators that allow us to propose this advancement. (AU)

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