Potassium Channels Regulate Cholecystokinin Secretion in STC-1 Cells

Snow, N. D.; Mangel, Allen W.; Sharara, Ala I.; Liddle, Roger A.

doi:10.1006/bbrc.1993.2196

Cited by 12 publications

(6 citation statements)

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“…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: 95%

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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: 95%

“…*P Ͻ 0.001. also express L-type calcium channels. Bombesin, sodium oleate, phenylalanine, barium chloride, and PMA are all potent CCK secretagogues for STC-1 cells (6,29,30,58,59), whereas glucose is a very weak stimulant (27). Inhibition of L-type calcium channel activity prevented secretagogue-stimulated CCK release.…”

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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“…By immunofluorescent staining, using CCK-specific antisera, over 95% of cultured STC-1 cells stained positively for CCK (28). STC-1 cells are intestinal in origin, contain high amounts of immunoreactive and bioactive CCK, and have many properties of native CCK cells including responsiveness to secretagogues such as bombesin, ␤-agonists, cAMP analogs, calcium ionophores, and membrane-depolarizing concentrations of KCl (6,29,(40)(41)(42). Therefore, STC-1 cells demonstrate regulated secretion that appears analogous to I cells and thus provide a unique model for studies of CCK secretion.…”

Section: Discussionmentioning

confidence: 99%

“…Radioimmunoassay of CCK. CCK release was measured by a sensitive and specific radioimmunoassay as previously described using antiserum #9322 (28,29,(40)(41)(42).…”

Section: Preparation Of Human Intestinal Mucosal Cellsmentioning

confidence: 99%

Luminal CCK-releasing factor stimulates CCK release from human intestinal endocrine and STC-1 cells

Wang

Prpic

Green

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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CCK is secreted into the blood from intestinal endocrine cells following ingestion of a meal. Recently, it has been demonstrated that the ability of certain foods to stimulate CCK release is mediated by endogenously produced CCK-releasing factors. A newly discovered luminal CCK-releasing factor (LCRF) is secreted into the intestine, where it stimulates CCK secretion. However, the mechanism whereby LCRF affects intestinal epithelial cells is unknown. The current study was designed to determine whether LCRF has a direct effect on CCK cells to stimulate hormone secretion. In dispersed human intestinal mucosal cells, LCRF (5-200 nM) significantly stimulated CCK release in a concentration-dependent manner. This stimulatory effect was absent in calcium-free media and was inhibited by the L-type calcium-channel blockers diltiazem and nifedipine. To examine direct cellular effects of LCRF on CCK cells, further studies were conducted in the CCK-containing enteroendocrine cell line STC-1. As in native cells, LCRF significantly stimulated CCK release from STC-1 cells in a calcium-dependent manner. In cells loaded with a calcium-sensitive dye, LCRF stimulation produced a rapid increase in intracellular calcium. To examine the electrophysiological basis for this stimulation, whole cell recordings were made from STC-1 cells. Whole cell calcium currents were identified under basal conditions; moreover, calcium-channel activity was increased by LCRF. These studies demonstrate that 1) LCRF has a direct effect on human intestinal cells to stimulate CCK secretion, 2) stimulated hormone release is calcium dependent, and 3) LCRF activates calcium currents in CCK cells, which leads to CCK secretion.

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“…Recently, an intestinal CCK-producing cell line (STC-1) was developed that secretes several gastrointestinal hormones, of which CCK is the most abundant (112,113). STC-1 cells have been used as a model for intestinal CCK secretion because identical stimuli release CCK from dispersed native intestinal cells and STC-1 cells (105,111,(114)(115)(116). Electrophysiological studies have been performed using STC-1 cells, which provide insight into the signal transduction pathways that are linked to ion channel activity and CCK secretion.…”

Section: Role Of Ion Channels In Cck Secretionmentioning

confidence: 99%

Cholecystokinin Cells

Liddle

1997

Annu. Rev. Physiol.

253

196

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Cholecystokinin (CCK) is an important hormonal regulator of the digestive process. CCK cells are concentrated in the proximal small intestine, and hormone is secreted into the blood upon the ingestion of food. The physiological actions of CCK include stimulation of pancreatic secretion and gallbladder contraction, regulation of gastric emptying, and induction of satiety. Therefore, in a highly coordinated manner, CCK regulates the ingestion, digestion, and absorption of nutrients. CCK is produced by two separate cell types: endocrine cells of the small intestine and various neurons in the gastrointestinal tract and central nervous system. Accordingly, CCK can function as either a hormone or a neuropeptide. This review focuses on the physiology of the CCK cell in the intestine and, in particular, on how the CCK cell is regulated to secrete its hormone product. The effects of ingested nutrients on the CCK cell and the intracellular messenger systems involved in controlling secretion are reviewed. A summary is provided of recent studies examining the electrophysiological properties of CCK cells and newly discovered proteins that act as releasing factors for CCK, which mediate feedback pathways critical for regulated secretion in the intact organism.

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Potassium Channels Regulate Cholecystokinin Secretion in STC-1 Cells

Cited by 12 publications

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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

Luminal CCK-releasing factor stimulates CCK release from human intestinal endocrine and STC-1 cells

Cholecystokinin Cells

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Potassium Channels Regulate Cholecystokinin Secretion in STC-1 Cells

Cited by 12 publications

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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

Luminal CCK-releasing factor stimulates CCK release from human intestinal endocrine and STC-1 cells

Cholecystokinin 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