Iptakalim, a Vascular ATP-Sensitive Potassium (KATP) Channel Opener, Closes Rat Pancreatic β-Cell KATP Channels and Increases Insulin Release

2007 ◽  
Vol 322 (2) ◽  
pp. 871-878 ◽  
Author(s):  
Naoko Misaki ◽  
Xia Mao ◽  
Yu-Fung Lin ◽  
Sechiko Suga ◽  
Guo-Hui Li ◽  
...  
Keyword(s):  
Insulin Release ◽  
Katp Channel ◽  
Katp Channels ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Channel Opener ◽  
Katp Channel Opener

scholarly journals The KATP channel opener, nicorandil, ameliorates brain damage by modulating synaptogenesis after ischemic stroke

PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0246019
Author(s):  
Yuanzheng Zhao ◽  
Zhuoying Yang ◽  
Yuanhong He ◽  
Ruonan Sun ◽  
Heping Yuan
Keyword(s):  
Cerebral Infarction ◽  
Brain Damage ◽  
Katp Channel ◽  
Infarct Volume ◽  
Katp Channels ◽  
Neurological Deficits ◽  
Nuclear Antigen ◽  
Protective Effects ◽  
Channel Opener ◽  
Katp Channel Opener

With population growth and aging, more and more patients with cerebral infarction have varying degrees of disability. ATP-sensitive potassium (KATP) channels regulate many cellular functions by coupling metabolic status with cell membrane electrical activity. Nicorandil (N-(2-hydroxyethyl)-nicotinamide nitrate) is the first KATP channel opener approved for clinical use. It has been reported that it might exert protective effects on the cerebral infarction by increasing cerebral blood flow and reducing inflammation. However, only a few studies explored its role in synaptogenesis. We made the rat model of middle cerebral artery occlusion (MCAO). Nicorandil was administered to rats via oral administration immediately after the surgery at a dose of 7.5 mg/kg and then daily for the next days. Infarct volume, cerebral edema, neurological deficits, cognitive impairment, and the level of Synaptophysin (SYP)、Growth associated protein-43 (GAP43) and neuronal nuclear antigen (NeuN) levels were measured to evaluate the effect of nicorandil. Our data showed that nicorandil treatment could decrease brain damage, improve learning and memory, and increase SYP、GAP43 and NeuN level. Taken together, we propose that nicorandil, as an opener of the KATP channel, provides a neuroprotective role in MCAO by promoting synaptic connections.

Diabetes prevention by a novel β cell-selective KATP channel opener, NNC55-0118, in OLETF rat

2000 ◽  
Vol 50 ◽  
pp. 383
Author(s):  
Toru Aizawa ◽  
John B Hansen ◽  
Richard D Carr ◽  
Christian L Brand ◽  
Mitsuhisa Komatsu ◽  
...  
Keyword(s):  
Katp Channel ◽  
Diabetes Prevention ◽  
Β Cell ◽  
Channel Opener ◽  
Katp Channel Opener ◽  
Oletf Rat

The agouti gene product stimulates pancreatic β-cell Ca2+ signaling and insulin release

1999 ◽  
Vol 1 (1) ◽  
pp. 11-19 ◽  
Author(s):  
B. Z. XUE ◽  
W. O. WILKISON ◽  
R. L. MYNATT ◽  
N. MOUSTAID ◽  
M. GOLDMAN ◽  
...  
Keyword(s):  
Gene Product ◽  
Insulin Release ◽  
Fold Increase ◽  
Cell Types ◽  
Human Pancreas ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Agouti Protein ◽  
Intracellular Ca ◽  
Agouti Gene

Xue, B. Z., W. O. Wilkison, R. L. Mynatt, N. Moustaid, M. Goldman, and M. B. Zemel. The agouti gene product stimulates pancreatic β-cell Ca2+ signaling and insulin release. Physiol. Genomics 1: 11-19, 1999.—Ubiquitous expression of the mouse agouti gene results in obesity and hyperinsulinemia. Human agouti is expressed in adipose tissue, and we found recombinant agouti protein to stimulate lipogenesis in adipocytes in a Ca2+-dependent fashion. However, adipocyte-specific agouti transgenic mice only became obese in the presence of hyperinsulinemia. Because intracellular Ca2+ concentration ([Ca2+]i) is a primary signal for insulin release, and we have shown agouti protein to increase [Ca2+]i in several cell types, we examined the effects of agouti on [Ca2+]i and insulin release. We demonstrated the expression of agouti in human pancreas and generated recombinant agouti to study its effects on Ca2+ signaling and insulin release. Agouti (100 nM) stimulated Ca2+ influx, [Ca2+]i increase, and a marked stimulation of insulin release in two β-cell lines (RIN-5F and HIT-T15; P < 0.05). Agouti exerted comparable effects in isolated human pancreatic islets and β-cells, with a 5-fold increase in Ca2+ influx ( P < 0.001) and a 2.2-fold increase in insulin release ( P < 0.01). These data suggest a potential role for agouti in the development of hyperinsulinemia in humans.

scholarly journals Acyl-Ghrelin Influences Pancreatic β-Cell Function by Interference with KATP Channels

Diabetes ◽  
2020 ◽  
pp. db200231
Author(s):  
Julia Kaiser ◽  
Peter Krippeit-Drews ◽  
Gisela Drews
Keyword(s):  
Cell Function ◽  
Katp Channels ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Β Cell Function ◽  
Acyl Ghrelin

Interaction between thiol-modifying agents and P1075, a KATP channel opener, in rat isolated aorta

1997 ◽  
Vol 356 (4) ◽  
pp. 467-474 ◽  
Author(s):  
Claudia Linde ◽  
Cornelia Löffler ◽  
Christina Kessler ◽  
U. Quast
Keyword(s):  
Katp Channel ◽  
Channel Opener ◽  
Isolated Aorta ◽  
Katp Channel Opener

Life and death decisions of the pancreatic β-cell: the role of fatty acids

2006 ◽  
Vol 112 (1) ◽  
pp. 27-42 ◽  
Author(s):  
Philip Newsholme ◽  
Deirdre Keane ◽  
Hannah J. Welters ◽  
Noel G. Morgan
Keyword(s):  
Fatty Acids ◽  
Insulin Release ◽  
Chronic Exposure ◽  
Cell Function ◽  
Pancreatic Β Cell ◽  
Β Cells ◽  
Β Cell ◽  
Endogenous Fatty Acid ◽  
Gene And Protein Expression ◽  
Β Cell Function

Both stimulatory and detrimental effects of NEFAs (non-esterified fatty acids) on pancreatic β-cells have been recognized. Acute exposure of the pancreatic β-cell to high glucose concentrations and/or saturated NEFAs results in a substantial increase in insulin release, whereas chronic exposure results in desensitization and suppression of secretion, followed by induction of apoptosis. Some unsaturated NEFAs also promote insulin release acutely, but they are less toxic to β-cells during chronic exposure and can even exert positive protective effects. Therefore changes in the levels of NEFAs are likely to be important for the regulation of β-cell function and viability under physiological conditions. In addition, the switching between endogenous fatty acid synthesis or oxidation in the β-cell, together with alterations in neutral lipid accumulation, may have critical implications for β-cell function and integrity. Long-chain acyl-CoA (formed from either endogenously synthesized or exogenous fatty acids) controls several aspects of β-cell function, including activation of specific isoenzymes of PKC (protein kinase C), modulation of ion channels, protein acylation, ceramide formation and/or NO-mediated apoptosis, and transcription factor activity. In this review, we describe the effects of exogenous and endogenous fatty acids on β-cell metabolism and gene and protein expression, and have explored the outcomes with respect to insulin secretion and β-cell integrity.

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