title: Selenium acts as an insulin-like molecule for the down-regulation of diabetic symptoms via endoplasmic reticulum stress and insulin signalling proteins in diabetes-induced non-obese diabetic mice.
abstract: To investigate whether selenium (Sel) treatment would impact on the onset of diabetes,we examined serum biochemical components including glucose and insulin,endoplasmic reticulum (ER) stress and insulin signalling proteins, hepatic C/EBP-homologous protein (CHOP) expression and DNA fragmentation in diabetic and non- diabetic conditions of non-obese diabetic (NOD) mice. We conclude that (i) Sel treatment induced insulin-like effects in lowering serum glucose level in Sel-treated NOD mice, (ii) Sel-treated mice had significantly decreased serum biochemical components associated with liver damage and lipid metabolism, (iii) Sel treatment led to the activation of the ER stress signal through the phosphorylation of JNK and eIF2 protein and insulin signal mechanisms through the phosphorylation of Akt and PI3 kinase, and (iv) Sel-treated mice were significantly relieved apoptosis of liver tissues indicated by DNA fragmentation assay in the diabetic NOD group. These results suggest that Sel compounds not only serve as insulin-like molecules for the downregulation of glucose level and the incidence of liver damage, but may also have the potential for the development of new drugs for the relief of diabetes by activating the ER stress and insulin signalling pathways.
authors.affiliation: Laboratory Animal Resources Team, National Institute of Toxicological Research, Korea FDA, Seoul 122-704, Korea. dyhwang@kfda.go.kr
authors.forename: Daeyoun
authors.initials: D
authors.lastname: Hwang
authors.forename: Sujin
authors.initials: S
authors.lastname: Seo
authors.forename: Yongkyu
authors.initials: Y
authors.lastname: Kim
authors.forename: Chuelkyu
authors.initials: C
authors.lastname: Kim
authors.forename: Sunbo
authors.initials: S
authors.lastname: Shim
authors.forename: Seungwan
authors.initials: S
authors.lastname: Jee
authors.forename: Suhae
authors.initials: S
authors.lastname: Lee
authors.forename: Mikyong
authors.initials: M
authors.lastname: Jang
authors.forename: Minsun
authors.initials: M
authors.lastname: Kim
authors.forename: Suyoun
authors.initials: S
authors.lastname: Yim
authors.forename: Sang-Koo
authors.initials: SK
authors.lastname: Lee
authors.forename: Byeongcheol
authors.initials: B
authors.lastname: Kang
authors.forename: Insurk
authors.initials: I
authors.lastname: Jang
authors.forename: Jungsik
authors.initials: J
authors.lastname: Cho
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight / Q000187:drug effects; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism*; D015536:Down-Regulation / Q000187:drug effects*; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D051379:Mice; D016688:Mice, Inbred NOD; D012643:Selenium / Q000494:pharmacology*; D015398:Signal Transduction
chemical_list: D001786:Blood Glucose; D007328:Insulin; D012643:Selenium