Insulin occludes leptin activation of ATP-sensitive K+channels in rat CRI-G1 insulin secreting cells
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چکیده
منابع مشابه
Leptin signalling in pancreatic islets and clonal insulin-secreting cells.
Leptin is a cytokine secreted from adipose tissue at a rate commensurate with the size of the body's fat stores. In addition to its anorectic and thermogenic central actions, leptin is known to act on peripheral tissues, including the pancreatic beta-cell where it inhibits insulin secretion and reduces insulin transcript levels. However, the role of leptin signalling through its full-length rec...
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The Department of Biomedical Science, The University, Western Bank, Sheffield. S10 2TN. patches. However, when exactly the same protocol was carried out cn patches of membrane excised from cells pre-treated overnight with 1 M PMA, pdymyxin-B induced Mock was readily reversible (n=8). There is therefore a marked difference in the mechanism of action of polymyxin B on K+AW channels in the presenc...
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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...
متن کاملLeptin suppression of insulin secretion by the activation of ATP-sensitive K+ channels in pancreatic beta-cells.
In the genetic mutant mouse models ob/ob or db/db, leptin deficiency or resistance, respectively, results in severe obesity and the development of a syndrome resembling NIDDM. One of the earliest manifestations in these mutant mice is hyperinsulinemia, suggesting that leptin may normally directly suppress the secretion of insulin. Here, we show that pancreatic islets express a long (signal-tran...
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In the genetic mutant mouse models ob/ob or db/db, leptin deficiency or resistance, respectively, results in severe obesity and the development of a syndrome resembling NIDDM. One of the earliest manifestations in these mutant mice is hyperinsulinemia, suggesting that leptin may normally directly suppress the secretion of insulin. Here, we show that pancreatic islets express a long (signal-tran...
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ژورنال
عنوان ژورنال: The Journal of Physiology
سال: 1998
ISSN: 0022-3751
DOI: 10.1111/j.1469-7793.1998.695bg.x