Abstract
Diabetes Mellitus (DM1 or DM2) is defined as a syndrome of chronic hyperglycemia due to the lack of insulin production that results from the reduction of beta cell mass which, in turn, originated from an increase in cell apoptosis and/or deficient beta cell regeneration. In DM2, reduction of beta cell mass is frequently accompanied by an increase in insulin resistance in muscle, adipose, and hepatic tissues. Despite the enormous amount of information present in the literature concerning the diabetic syndrome, the molecular mechanisms underlying this syndrome is not completely known. Following our preceding studies, in the present Project we will study the mechanisms responsible for the loss of the mass and functionality of pancreatic islets in different animal models (protein malnutrition, obesity, dislipidemia, and induced DM2) and cell types. We will also study the mechanisms involved in the increase in islet cell mass in different periods of life (fetal, neonatal and pregnancy). In the former, the focus will be on the participation of ER stress, alteration in Ca2+ handling, and increase in the oxidative stress. In the later, the attention will centered on the signaling pathways that control the increase in mass and functionality of the pancreatic islets as well as on possible benefits to the islets by amino acids supplementation or by the use of peptides that showed previously to be able to restore islet cell viability. (AU)
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