ATP enhances exocytosis of insulin secretory granules in pancreatic islets under Ca2+-depleted condition
Autor: | Mihoko Takehiro, Dai Shimono, Yuichiro Yamada, Yutaka Seino, Makiko Shimodahira, Rieko Kominato, Shimpei Fujimoto, Shogo Funakoshi, Yuichi Nishi, Yo Aramaki, Razvan Gheorghe Radu, Koichiro Nabe, Eri Mukai |
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Rok vydání: | 2005 |
Předmět: |
Male
medicine.medical_specialty GTP' Endocrinology Diabetes and Metabolism medicine.medical_treatment Adenylyl Imidodiphosphate chemistry.chemical_element Calcium Exocytosis Islets of Langerhans Adenosine Triphosphate Endocrinology Internal medicine Insulin receptor substrate Insulin Secretion Internal Medicine Animals Insulin Medicine Rats Wistar Protein kinase A Protein kinase C business.industry Pancreatic islets General Medicine Rats Kinetics medicine.anatomical_structure chemistry Tetradecanoylphorbol Acetate business |
Zdroj: | Diabetes Research and Clinical Practice. 69:216-223 |
ISSN: | 0168-8227 |
DOI: | 10.1016/j.diabres.2005.01.010 |
Popis: | Glucose and other nutrients have been shown to stimulate insulin release from pancreatic islets under Ca2+-depleted condition when protein kinase A (PKA) and protein kinase C (PKC) are activated simultaneously. We investigated the role of metabolic nucleotide signals including ATP, ADP, and GTP in exocytosis of insulin secretory granules under Ca2+-depleted condition using electrically permeabilized rat islets. ATP under PKC activation augmented insulin release concentration-dependently by 100 nM 12-O-tetradecanoyl-phorbol-13-acetate (TPA) in Ca2+-depleted condition, while ADP could not suppress ATP-dependent insulin release in this condition. Neither GTP nor activated PKA in the absence of PKC activation increased insulin release under Ca2+-depleted condition in the presence of ATP, but both enhanced insulin secretion in the presence of ATP when PKC was activated. In conclusion, activated PKC and the presence of ATP both are required in the insulin secretory process under Ca2+-depleted condition. While PKA activation and GTP cannot substitute for PKC activation and ATP, respectively, under Ca2+-depleted condition, they enhance ATP-dependent insulin secretion when PKC is activated. |
Databáze: | OpenAIRE |
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