Mg2+-dependent inhibition of KATP by sulphonylureas in CRI-G1 insulin-secreting cells
نویسندگان
چکیده
منابع مشابه
differentiation of human embryonic stem cells into insulin- secreting cells
introduction: type i diabetes mellitus is caused by autoimmune destruction of the insulin-producing β-cells. a new potential method for curing the disease is transplantation of differentiated insulin- secreting cells from human embryonic stem cells. methods: human embryonic stem cell lines (royan h1) were used to produce embryoid bodies. differentiation carried out by growth factor-mediated sel...
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The gap-junction protein connexin36 (Cx36) contributes to control the functions of insulin-producing cells. In this study, we investigated whether the expression of Cx36 is regulated by glucose in insulin-producing cells. Glucose caused a significant reduction of Cx36 in insulin-secreting cell lines and freshly isolated pancreatic rat islets. This decrease appeared at the mRNA and the protein l...
متن کامل2-Ketoisocaproate transport in insulin-secreting cells.
The transport of the nutrient secretagogue 2-ketoisocaproate (KIC) was studied in isolated rat pancreatic islets and in the HIT-T15 insulinoma cell line using an oil-filtration technique. In both islets and HIT-T15 cells, KIC uptake was a slow process, not reaching equilibrium within 10 min KIC transport was not dependent upon Na+ in the medium, was not inhibited by alpha-cyano-4-hydroxycinnama...
متن کاملSulfonylurea binding to a low-affinity site inhibits the Na/K-ATPase and the KATP channel in insulin-secreting cells
We have used hamster insulinoma tumor (HIT) cells, an insulin-secreting tumor cell line, to investigate modulation of the Na/K-ATPase and of the ATP-sensitive K channel (K(ATP)) by the sulfonylurea glyburide. Membrane proteins from cells cultured in RPMI with 11 mM glucose have at least two glyburide receptor populations, as evidenced by high and low binding affinity constants, (K(d) = 0.96 and...
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ژورنال
عنوان ژورنال: British Journal of Pharmacology
سال: 1994
ISSN: 0007-1188
DOI: 10.1111/j.1476-5381.1994.tb14783.x