The Effect Of Dietary Selenium And VitaminE Deficiency On Selenoprotein Genes Expression In Pancreas Of Broiler

Selenium(Se) plays important roles on maintaining the function of pancreas, and chicken is the animal which panceas is extremely susceptible to dietary Se deficiency, Se deficiency could cause pancreatic degeneration, necrosis, atrophy and fibrosis, however, the biological mechanism is unclear. There is an interaction between Se and VE, Se-deficient dietary accompany with VE deficiency will aggravate the animal pathological symptoms. In this research we take broiler as research materials and study the effect of dietary Se and VE deficiency on production performance, physiological and biochemical indexes of the chicken, also pancreatic morphology, structure of pancreatic cell and Selenoprotein genes expression in pancreas. The results may provide clues about the biological mechanisms of Se and VE on maintaining the pancreatic function, also the results were expected to be helped for pathogenic mechanism investigation of major diseases concerning human health (such as diabetes,pancreatic cancer).In this experiment, the basal diet (BD) was composed of corn and soybean meal produced in severe Se-deficient area of Sichuan (Hanyuan Mountain). Four groups of day-old Arbor Acre broiler chicks (n=60/group) were fed a corn-soy basal diet (BD,14μg Se/kg; VE 8.21mg/kg; and not supplemented with Se or vitamin E), or the BD+ rac-a-tocopheryl acetate at 50 mg/kg, Se(as sodium selenite) at 0.3 mg/kg, or both of two nutrients for 6 wk. ED and other classical Se-deficient diseases and mortality of broilers were recoreded. At 28 d, broilers (n=5/group) were killed, blood and pancreas samples were collected for Se and VE concentrations assayed, also pancreas pathological morphology were investigated and the affects of dietary Se or VE deficiency on 15 selenoprotein genes expression in pancreas were assayed by RT-qPCR.The results were as follow.1. The Se-VE deficient group appeared ED, dyskinesia, diarrhea and other symptoms early in 3wk. Autopsy showed subcutaneous hemorrhage and a greenish, gelatinous edema under the skin of dependent portions of the body-always the breast sometimes under the wings, and down the legs (incidence rate 93%), meanwhile bleeders in chest and leg muscle of different extent (incidence rate 73.3%), the Se-deficient group also appear similar symptoms, however, the morbidity and degree are lower. The VE-deficient group and the contorl group appeared nomorally.2. Pancreas of se-ve deficient group turn to thinner, narrower, smaller (Incidence rate 13.3%). other groups are nomoral. The length of pancreas in unsupplemented with Se groups(-Se-VE,-Se+VE) is shorter than that supplemented groups(+Se-VE,-Se+VE) (P<0.05). Pancreatic organ index of Se-VE deficient group is lower than the control group(P<0.05), no difference among other groups. Pathology of Se-VE deficient group showed structural changes in pancreatic cells in 23 d, then showed acinar structural disorder, many cytoplasmic vacuoles in acinar cells in 28 d. the Se-deficient group just appeared a little cytoplasmic vacuoles. Whereas the other groups appeared nomorally.3. Se concentration were elevated by supplementations of both Se and VE(P<0.05) in plasma and pancreas, plasma VE concentration were increased only by the VE supplemcntation(P<0.05).4. The final body weight and daily gain of broilers were decreased by Se and VE deficiency, body weight of the control group higher than other three groups from 1wk to 4wk(P<0.05). Daily feed intake were decreased only by dietary Se deficiency(P<0.05).5. Quantitative results showed that:①Broilers fed Se/VE-deficient and both deficiency diets had lower pancreatic mRNA levels of Gpx1, Gpx4, TR1, TR2, TR3, Sepw1, Sepp1, Selo, Sels, Selt, Sepx1, Seli, Sepn1, Sep1, Selk than control diet.②Se and VE had an interaction on mRNA levels of 10 Selenoprotein genes(Gpx1, Gpx4, Sepw1, Sepp1, Selo, Sels, Sell, Sepx1, Seli, TR2)(P<0.05). When add VE in low Se levels, there are 6 Selenoprotein genes(Gpx1, Gpx4, Sepw1, Selo, Sepx1, TR2) been affected significantly (P<0.05); When add VE in normol Se levels, there are 9 Selenoprotein genes(Gpx1, Gpx4, Sepw1, Sepp1, Selo, Sels, Selt, Sepx1, Seli, TR2) been affected significantly(P<0.05); When add Se in low VE levels, there are 5 Selenoprotein genes(Gpx4, Sepw1, Sepp1, Sepx1, TR2) been affected significantly(P<0.05); When add Se in normol VE levels, there are 9 Selenoprotein genes(Gpxl, Gpx4, Sepw1, Sepp1, Selo, Sell, Sepxl, Seli, TR2) been affected significantly(P<0.05).③VE exerted a main effect on 3 Selenoprotein genes(TR1, Sepn1, Sepl5) (P<0.01), compared with the control group, the other three groups were down-regulated of different degree.④Se exerted a main effect on 2 Selenoprotein genes(TR1, Selk)(P<0.01), compared with the control group, the other three groups were down-regulated of different degree.⑤Compared with Se/VE deficient group, Selenoprotein genes expression were up-regulated of Se-VE deficient group.Conclusion:growth performance, pancreatic organ index, pancreatic structures were affected significantly by dietary Se and VE deficiencies. RT-qPCR results showed:the expression of Selenoprotein genes(Gpx1, Gpx4, TR1, TR2, TR3, Sepw1, Seppl, Selo, Sels, Sell, Sepx1, Seli, Sepn1, Sep15, Selk) were down-regulated, indicated that these genes plays an important role on maintain pancreatic normal function.