{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,17]],"date-time":"2026-05-17T22:36:12Z","timestamp":1779057372410,"version":"3.51.4"},"reference-count":79,"publisher":"American Diabetes Association","issue":"5","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2001,5,1]]},"abstract":"<jats:p>Insulin-secreting pancreatic islet \u03b2-cells possess anion-permeable Cl\u2212 channels (ICl,islet) that are swelling-activated, but the role of these channels in the cells is unclear. The Cl\u2212 channel blockers 4,4\u2032-diisothiocyanostilbene-2,2\u2032-disulfonic acid (DIDS) and niflumic acid were evaluated for their ability to inhibit ICl,islet in clonal \u03b2-cells (HIT cells). Both drugs blocked the channel, but the blockade due to niflumic acid was less voltage-dependent than the blockade due to DIDS. HIT cell volume initially increased in hypotonic solution and was followed by a regulatory volume decrease (RVD). The addition of niflumic acid and, to a lesser extent, DIDS to the hypotonic solution potentiated swelling and blocked the RVD. In isotonic solution, niflumic acid produced swelling, suggesting that islet Cl\u2212 channels are activated under basal conditions. The channel blockers glyburide, gadolinium, or tetraethylammonium-Cl did not alter hypotonic-induced swelling or volume regulation. The Na\/K\/2Cl transport blocker furosemide produced cell shrinkage in isotonic solution and blocked cell swelling normally induced by hypotonic solution. Perifused HIT cells secreted insulin when challenged with hypotonic solutions. However, this could not be completely attributed to ICl,islet-mediated depolarization, because secretion persisted even when Cl\u2212 channels were fully blocked. To test whether blocker-resistant secretion occurred via a distal pathway, distal secretion was isolated using 50 mmol\/l potassium and diazoxide. Under these conditions, glucose-dependent secretion was blunted, but hypotonically induced secretion persisted, even with Cl\u2212 channel blockers present. These results suggest that \u03b2-cell swelling stimulates insulin secretion primarily via a distal ICl,islet-independent mechanism, as has been proposed for KATP-independent glucose- and sulfonylurea-stimulated insulin secretion. Reverse transcriptase\u2013polymerase chain reaction of HIT cell mRNA identified a CLC-3 transcript in HIT cells. In other systems, CLC-3 is believed to mediate swelling-induced outwardly rectifying Cl\u2212 channels. This suggests that the proximal effects of swelling to regulate cell volume may be mediated by CLC-3 or a closely related Cl\u2212 channel.<\/jats:p>","DOI":"10.2337\/diabetes.50.5.992","type":"journal-article","created":{"date-parts":[[2007,3,6]],"date-time":"2007-03-06T19:04:22Z","timestamp":1173207862000},"page":"992-1003","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":28,"title":["Chloride Channels Regulate HIT Cell Volume but Cannot Fully Account for Swelling-Induced Insulin Secretion"],"prefix":"10.2337","volume":"50","author":[{"given":"Tracie A.","family":"Kinard","sequence":"first","affiliation":[{"name":"Departments of Pharmacology and Toxicology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paulette B.","family":"Goforth","sequence":"additional","affiliation":[{"name":"Departments of Pharmacology and Toxicology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qing","family":"Tao","sequence":"additional","affiliation":[{"name":"Departments of Pharmacology and Toxicology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mary E.","family":"Abood","sequence":"additional","affiliation":[{"name":"Departments of Pharmacology and Toxicology"},{"name":"Forbes Norris ALS Research Center, California Pacific Medical Center, San Francisco, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeanette","family":"Teague","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolism and Nutrition Department of Medicine, School of Medicine, University of Washington, Seattle, Washington"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Leslie S.","family":"Satin","sequence":"additional","affiliation":[{"name":"Departments of Pharmacology and Toxicology"},{"name":"Department of Physiology"},{"name":"Medicine (Endocrinology), Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1167","reference":[{"key":"2022031207175845100_R1","doi-asserted-by":"crossref","unstructured":"Ashcroft FM, Rorsman P: Electrophysiology of the pancreatic \u03b2-cell. 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