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Title: Role of aryl hydrocarbon receptor nuclear translocator in K{sub ATP} channel-mediated insulin secretion in INS-1 insulinoma cells

Journal Article · · Biochemical and Biophysical Research Communications
;  [1];  [1];  [2];  [3];  [1];  [1]
  1. Department of Physiology, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-gu, Seoul 110-799 (Korea, Republic of)
  2. Department of Pharmacology, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-gu, Seoul 110-799 (Korea, Republic of)
  3. Department of Internal Medicine, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-gu, Seoul 110-799 (Korea, Republic of)

Aryl hydrocarbon receptor nuclear translocator (ARNT) has been known to participate in cellular responses to xenobiotic and hypoxic stresses, as a common partner of aryl hydrocarbon receptor and hypoxia inducible factor-1/2{alpha}. Recently, it was reported that ARNT is essential for adequate insulin secretion in response to glucose input and that its expression is downregulated in the pancreatic islets of diabetic patients. In the present study, the authors addressed the mechanism by which ARNT regulates insulin secretion in the INS-1 insulinoma cell line. In ARNT knock-down cells, basal insulin release was elevated, but insulin secretion was not further stimulated by a high-glucose challenge. Electrophysiological analyses revealed that glucose-dependent membrane depolarization was impaired in these cells. Furthermore, K{sub ATP} channel activity and expression were reduced. Of two K{sub ATP} channel subunits, Kir6.2 was found to be positively regulated by ARNT at the mRNA and protein levels. Based on these results, the authors suggest that ARNT expresses K{sub ATP} channel and by so doing regulates glucose-dependent insulin secretion.

OSTI ID:
21255897
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 379, Issue 4; Other Information: DOI: 10.1016/j.bbrc.2009.01.004; PII: S0006-291X(09)00022-9; Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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