Islet ß-cell-produced NUCB2/nesfatin-1 maintains insulin secretion and glycemia along with suppressing UCP-2 in ß-cells.
J Physiol Sci
; 69(5): 733-739, 2019 Sep.
Article
em En
| MEDLINE
| ID: mdl-31228099
ABSTRACT
Nesfatin-1 is a hypothalamic anorexigenic peptide processed from nucleobindin 2 (NUCB2). Central and peripheral administration of NUCB2/nesfatin-1 enhances glucose metabolism and insulin release. NUCB2/nesfatin-1 is also localized in pancreatic islets, while its function remains unknown. To explore the role of pancreatic ß-cell-produced NUCB2/nesfatin-1, we developed pancreatic ß-cell-specific NUCB2 knockout (ßNUCB2 KO) mice and NUCB2 gene knockdown (shNUCB2) MIN6 ß-cell line. In ßNUCB2 KO mice, casual blood glucose was elevated from 12 weeks of age. In a glucose tolerance test at 12 weeks, insulin secretion at 15 min was reduced and blood glucose at 2 h increased in ßNUCB2 KO mice fasted 8 h. In islets isolated from ßNUCB2 KO mice, high glucose-stimulated insulin secretion (GSIS) was impaired. In shNUCB2 MIN6 cells, GSIS was reduced and UCP-2 mRNA expression was elevated. These results show impaired GSIS possibly associated with UCP-2 overexpression in NUCB2-silenced ß-cells, suggesting that ß-cell-produced NUCB2/nesfatin-1 maintains GSIS and thereby glycemia.
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MEDLINE
Assunto principal:
Glicemia
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Índice Glicêmico
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Células Secretoras de Insulina
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Proteína Desacopladora 2
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Secreção de Insulina
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Nucleobindinas
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Insulina
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article