The insulin secretion can be stimulated by many nutrients, neurotransmitters and peptide hormones, however, its main secretagogue is the glucose. Obesity and malnourishment are related to energetic homeostasis imbalance, leading to dysfunction of pancreatic beta-cells. Rodents submitted to protein malnourishment after weaning, shows alterations on insulin secretion process. It was observed many molecular alterations of glucose-induced insulin secretion (GIIS) caused by low protein diet. On the other hand, under protein malnourishment conditions, the alterations in the control of metabolites involved in GIIS modulation are still unknown. Nevertheless, evidences suggest that alterations in the coupling between the glycolytic pathway and mitochondrial metabolism, damaging ATP production and other metabolic coupling factors (MCFs) in the pancreatic beta-cells, resulting in changes on insulin secretion. The loss of coupling between glycolysis and mitochondrial metabolism has been pointed as one of the factors related to development of others diseases, as obesity and diabetes. Both low-calorie diets as hyperlipidic diets during important stages of development, induce a series of changes in glucose metabolism in pancreatic islets, however, the association between these two treatments have not yet been investigated. Therefore, the aim of this study is to investigate the molecular mechanisms involved in metabolic control of GIIS in malnourished animals subsequently induced to experimental obesity.
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