Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Hwang, D. et al.

Daeyoun Hwang, Sujin Seo, Yongkyu Kim, Chuelkyu Kim, Sunbo Shim, Seungwan Jee, Suhae Lee, Mikyong Jang, Minsun Kim, Suyoun Yim, Sang-Koo Lee, Byeongcheol Kang, Insurk Jang, Jungsik Cho,

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.

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.[1]

References

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. Hwang, D., Seo, S., Kim, Y., Kim, C., Shim, S., Jee, S., Lee, S., Jang, M., Kim, M., Yim, S., Lee, S.K., Kang, B., Jang, I., Cho, J. J. Biosci. (2007) [Pubmed]

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