Abstract： Objective To explore the effect of multiple organ dysfunction syndrome (MODS) on the ultra-structure and function of pancreatic beta cells and to provide a theoretical basis for clinical treatment of high blood glucose in patients with MODS. Method This study was performed in the Animal Department of Fujian Provincial Hospital, the Key Laboratory of Fujian Provincial Cardiovascular Institute, the Pathology Department of Fujian Provincial Hospital and in the Electron Microscopic Department of Fujian Medical University. Sixteen pathogen-free male Sprague-Dawley rots weighing 180 ～ 220 g, were selected and randomly divided into MODS group and control group (8 rats per group). MODS was induced by intraperitoneal injection with bacterium c oli and cutting the left legs. Rats in the control group received an intraperitoneal injection of an equivalent volume of sodium chloride. The MODS model was considered successful when two or more organs showed dysfunction 48 h after the injection. The blood glucose and plasma insulin levels were measured in the fasting state and in response to a glucose load. All data were analyzed using t tests. The plasma insulin concentration was analyzed after logarithmic transforma-tion. The ultrastructure of the pancreatic beta cells was observed under an electron microscope. The expression of Bax was determined immunohistochemically. Results The blood glucose during fasting, the blood glucose level 30 min after a glucose load and the expression of Bax were significantly in the MODS group compared with the con-trol group (P <0.01). In addition, the plasma insulin concentration level was insignificantly increased 30 min af-ter the glucose load in the MODS group (P < 0.01). Pathological uhrastructural changes were found, as follows: most pancreatic beta cells in the MODS group exhibited vacuole degeneration, some were necrotized, the mitochen-dria had swollen and the rough endoplasmic reticulum had expanded. Conclusions The uhltrastructure of the pan-creatic beta cells in the MODS rats shewed significant pathologic changes, with increased expression of Bax. These pathological changes may he responsible for the decreased insulin secretion, which caused the increased blood glu-cose levels.