Physiological And Immunological Effects Of Di-(2-ethylhexyl) Phthalate (Dehp) And A High Fat Diet (Hfd)in Glucose Homeostatic Organs In Balb/C Mice

Prolonged intake of a high-fat diet (HFD) and carbohydrate consumption was reported to stimulate the generation of reactive oxygen species with increased expression levels of several markers of inflammation. It was also suggested that increased exposure to environmental pollutants plays an important role in the increasing prevalence of type2diabetes. We evaluate the effects of di (2-ethylhexyl) phthalate (DEHP) on glucose metabolism, and inflammatory process; and the ability of vitamin E to suppress these deleterious effects in white adipose tissue (WAT), liver, and pancreas of mice fed high fat diet (HFD). Mice were treated with500mg/kg body weight DEHP while receiving an HFD. After4weeks, a group of mice received an oral dose of vitamin E. Ten weeks later, blood glucose, plasma insulin were assessed and then, mice were sacrificed and concentrations of Plasma triglyceride (TG), malondialdehyde (MDA), glutathione peroxydase (GPx), tumor necrosis factor (TNF)-a, interleukin (IL)-1β, and interferon (IFN)-y from WAT, liver, and pancreas were measured. Small pieces of liver and pancreas were removed and rinsed with saline. The tissues were fixed with formaldehyde and embedded in paraffin. Tissue sections were cut at thickness of2.5μm and stained with hematoxylin and eosin (HE) and image were captured using a Nikon microscope at (?)40magnification.HFD-fed mice decreased weight gain following DEHP and vitamin E supplementations. HFD-fed mice expressed high levels of glucose and insulin. However, HFD-fed, DEHP treated mice expressed much higher level of glucose and low insulin concentration; decreased glucose, and increased insulin levels following vitamin E supplementation. TNF-a, IL-1β, and IFN-γ levels decreased in WAT and liver following DEHP administration. However, TNF-a, and IL-1β levels increased in all organs while the IFN-y level decreased in WAT and pancreas following HFD-fed [7] and DEHP treatment. Vitamin E decreased cytokine levels in HFD-fed mice, in WAT and the liver, and did not affect cytokine levels in the pancreas. HFD-fed mice decreased levels of TG in blood serum following DEHP supplementation. However, following vitamin E supplementation, HFD-fed, DEHP exposed mice increased levels of TG. HFD-fed mice increased MDA, and GPx activity in liver, pancreas, and WAT as well as apoptosis or necrosis and decreased steatosis in liver following DEHP supplementation and vitamin E suppresses these effects in liver and pancreas except in WAT. In pancreas, HFD-fed mice increased insulitis and apoptosis or necrosis following DEHP supplementation. However, with vitamin E supplementation, HFD-fed, DEHP exposed mice increased lipid accumulation in non hormone secreting cells in pancreas.