Previous studies of our laboratory show that oxidative stress and mitochondrial dysfunction in heart, liver and diaphragm, associated with increased production of NO, are implicated in tissue damage during endotoxemia. Pancreas has been described to be affected in early-endotoxemic process, with acute inflammatory response and increases in the production of inflammatory cytokines and cellular apoptosis. However, its contribution in this complex systemic process has not been clarified yet. Besides, mitochondria are the main source of ATP and other biological molecules necessary for cellular and tissue recovery, so it is essential to maintain a suitable mitochondrial bioenergetics for the recovery from cellular, tissue and pancreatic organic damage in this syndrome. The aim of this work was to analyze the status of pancreatic mitochondrial function and dynamics in a rat model of low grade and severe endotoxemia. Experimental endotoxemia was induced in female Sprague Dawley rats (45days) by LPS 0.5 (0.5 mg/kg ip), LPS 8 (8 mg/kg ip) or control (vehicule ip). Assays were performed in pancreas 6h after the treatment. To evaluate mitochondrial function, mitochondrial ATP production was measured and was found significantly decreased (30%) in all LPS groups (control value: 70.4 ± 5 nmoles ATP/min mg protein, p <0.05). We evaluated the activity of mitochondrial respiratory chain complexes, observing a significant decrease of all the complexes evaluated for both LPS doses. This scenario was accompanied by an increased cytoplasmic production of O2●-. Finally, the expression levels of OPA1 (mitochondrial fusion protein) and DRP1 (mitochondrial fission protein) were increased, suggesting that mitochondrial dynamics is active during endotoxemia. Our results suggest that during endotoxemia increases the production of ROS by the activation of cytosolic NADPH oxidase, which could partially induce damage in pancreatic mitochondria. Furthermore, changes are triggered at the level of mitochondrial dynamics, probably as a cellular protective mechanism in order to recover mitochondrial function and cellular bioenergetics to restore the organic function of the pancreas.