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 |
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Authors: | 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 |
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Institution: | (1) Present address: Laboratory Animal Resources Team, National Institute of Toxicological Research, Korea FDA, Seoul, 122-704, Korea;(2) Center for Laboratory Animal Science, Hanyang University College of Medicine, 133-791 Hanyang, Korea;(3) Department of Experimental Animal Research, Clinical Research Institute, Seoul National University Hospital, Seoul, 110-744, Korea;(4) Department of Animal Science and Biotechnology, RAIC, Jinju National University, Jinju, 660-758, Korea |
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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. |
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Keywords: | Selenium ER stress insulin signal NOD lipid metabolism apoptosis |
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