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Melatonin-mediated intracellular insulin during 2-deoxy-D-glucose treatment is reduced through autophagy and EDC3 protein in insulinoma INS-1E cells

 
: Kim, Han Sung; Han, Tae-Young; Yoo, Yeong-Min

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Volltext (PDF; )

Oxidative medicine and cellular longevity 2016 (2016), Art. 2594703, 11 S.
ISSN: 1942-0900
ISSN: 1942-0994
Englisch
Zeitschriftenaufsatz, Elektronische Publikation
Fraunhofer IKTS ()

Abstract
2-DG triggers glucose deprivation without altering other nutrients or metabolic pathways and then activates autophagy via activation of AMPK and endoplasmic reticulum (ER) stress. We investigated whether 2-DG reduced intracellular insulin increased by melatonin via autophagy/EDC3 in insulinoma INS-1E cells. p-AMPK and GRP78/BiP level were significantly increased by 2-DG in the presence/absence of melatonin, but IRE1α level was reduced in 2-DG treatment. Levels of p85α, p110, p-Akt (Ser473, Thr308), and p-mTOR (Ser2481) were also significantly reduced by 2-DG in the presence/absence of melatonin. Mn-SOD increased with 2-DG plus melatonin compared to groups treated with/without melatonin alone. Bcl-2 was decreased and Bax increased with 2-DG plus melatonin. LC3II level increased with 2-DG treatment in the presence/absence of melatonin. Intracellular insulin production increased in melatonin plus 2-DG but reduced in treatment with 2-DG with/without melatonin. EDC3 was increased by 2-DG in the presence/absence of melatonin. Rapamycin, an mTOR inhibitor, increased GRP78/BiP and EDC3 levels in a dose-dependent manner and subsequently resulted in a decrease in intracellular production of insulin. These results suggest that melatonin-mediated insulin synthesis during 2-DG treatment involves autophagy and EDC3 protein in rat insulinoma INS-1E cells and subsequently results in a decrease in intracellular production of insulin.

: http://publica.fraunhofer.de/dokumente/N-410721.html