Characterization of ATP-Sensitive Potassium Channels in Intestinal, Cholecystokinin-Secreting Cells

Basavappa, Srisaila; Liddle, Roger A.; Mangel, Allen W.

doi:10.1006/bbrc.1994.2538

Cited by 7 publications

(7 citation statements)

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“…Patch-clamp studies have also demonstrated the presence of K ATP channels in parent STC-1 cells (2,28,30,58). Thus it has been proposed that they play a role in regulating CCK secretion (2,27,28). However, the results presented in this paper suggest that K ATP channels play, at best, a very minor role in regulating CCK secretion, since CCK-producing cells in vivo do not express detectable levels of Kir 6.1 or Kir 6.2.…”

Section: Discussionmentioning

confidence: 64%

“…This conclusion is consistent with our in vivo immunohistochemical studies indicating that gut L cells, like gut K cells, do not express detectable Kir 6.1 or Kir 6.2. Patch-clamp studies have also demonstrated the presence of K ATP channels in parent STC-1 cells (2,28,30,58). Thus it has been proposed that they play a role in regulating CCK secretion (2,27,28).…”

Section: Discussionmentioning

confidence: 99%

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Studies with GIP/Ins cells indicate secretion by gut K cells is K_ATPchannel independent

Wang¹,

M.‐Y.

Li³

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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K cells are a subpopulation of enteroendocrine cells that secrete glucose-dependent insulinotropic polypeptide (GIP), a hormone that promotes glucose homeostasis and obesity. Therefore, it is important to understand how GIP secretion is regulated. GIP-producing (GIP/Ins) cell lines secreted hormones in response to many GIP secretagogues except glucose. In contrast, glyceraldehyde and methyl pyruvate stimulated hormone release. Measurements of intracellular glucose 6-phosphate, fructose 1,6-bisphosphate, and pyruvate levels, as well as glycolytic flux, in glucose-stimulated GIP/Ins cells indicated that glycolysis was not impaired. Analogous results were obtained using glucose-responsive MIN6 insulinoma cells. Citrate levels increased similarly in glucose-treated MIN6 and GIP/Ins cells. Thus pyruvate entered the tricarboxylic acid cycle. Glucose and methyl pyruvate stimulated 1.4- and 1.6-fold increases, respectively, in the ATP-to-ADP ratio in GIP/Ins cells. Glyceraldehyde profoundly reduced, rather than increased, ATP/ADP. Thus nutrient-regulated secretion is independent of the ATP-dependent potassium (KATP) channel. Antibody staining of mouse intestine demonstrated that enteroendocrine cells producing GIP, glucagon-like peptide-1, CCK, or somatostatin do not express detectable levels of inwardly rectifying potassium (Kir) 6.1 or Kir 6.2, indicating that release of these hormones in vivo may also be KATP channel independent. Conversely, nearly all cells expressing chromogranin A or substance P and ∼50% of the cells expressing secretin or serotonin exhibited Kir 6.2 staining. Compounds that activate calcium mobilization were potent secretagogues for GIP/Ins cells. Secretion was only partially inhibited by verapamil, suggesting that calcium mobilization from intracellular and extracellular sources, independent from KATP channels, regulates secretion from some, but not all, subpopulations of enteroendocrine cells.

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Section: Discussionmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Studies with GIP/Ins cells indicate secretion by gut K cells is K_ATPchannel independent

Wang¹,

M.‐Y.

Li³

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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“…In STC-1 cells typical stimuli causing depolarization or increase in cAMP levels activate voltage-gated calcium channels leading to calcium influx and CCK secretion [22]. The L-type voltage-gated calcium channel blockers nimodipine and nifedipine have been previously shown to totally block the L-type voltage-gated channels activated by various stimuli in STC-1 cells in the same or even lower concentrations that used in this study [18,19,23,24].…”

Section: Discussionmentioning

confidence: 67%

TRPA1 channel activation induces cholecystokinin release via extracellular calcium

et al. 2007

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TRPA1 channels are non-selective cation channels activated by plant derived pungent products including allyl isothiocyanate (AITC) from mustard. Therefore, possible intestinal secretory functions of these channels were investigated. We detected TRPA1 mRNA in mouse and human duodenal mucosa and in intestinal mouse neuroendocrine STC-1 cells. Stimulation of STC-1 cells with AITC increased intracellular calcium ([Ca 2+ ] i ) and significantly stimulated cholecystokinin secretion by 6.7-fold. AITC induced cholecystokinin release was completely blocked by TRPA1 antagonist ruthenium red and depletion of extracellular calcium and reduced by 36% by nimodipine and nifedipine. This suggests that spices in our daily food might stimulate digestive functions.

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“…The identification of Kir6.2 and SUR1 by RT-PCR is consistent with the electrophysiological finding that the channels were sensitive to tolbutamide and diazoxide. K ATP channels have been detected previously in the poorly differentiated and multipotential CCK-secreting cell line STC-1, which also releases GIP and GLP-1 (31)(32)(33). CCK secretion from STC-1 cells was stimulated by 5 and 25 mmol/l glucose and by the nonspecific channel blocker disopyramide (31).…”

Section: Discussionmentioning

confidence: 80%

Glucose-Sensing in Glucagon-Like Peptide-1-Secreting Cells

Reimann

Gribble²

2002

Diabetes

254

231

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Characterization of ATP-Sensitive Potassium Channels in Intestinal, Cholecystokinin-Secreting Cells

Cited by 7 publications

References 0 publications

Studies with GIP/Ins cells indicate secretion by gut K cells is K_ATPchannel independent

Studies with GIP/Ins cells indicate secretion by gut K cells is K_ATPchannel independent

TRPA1 channel activation induces cholecystokinin release via extracellular calcium

Glucose-Sensing in Glucagon-Like Peptide-1-Secreting Cells

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Characterization of ATP-Sensitive Potassium Channels in Intestinal, Cholecystokinin-Secreting Cells

Cited by 7 publications

References 0 publications

Studies with GIP/Ins cells indicate secretion by gut K cells is KATPchannel independent

Studies with GIP/Ins cells indicate secretion by gut K cells is KATPchannel independent

TRPA1 channel activation induces cholecystokinin release via extracellular calcium

Glucose-Sensing in Glucagon-Like Peptide-1-Secreting Cells

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Studies with GIP/Ins cells indicate secretion by gut K cells is K_ATPchannel independent

Studies with GIP/Ins cells indicate secretion by gut K cells is K_ATPchannel independent