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Insulin secretion is stimulated as glucose rises from euglycemia, with incretin hormones modulating the secretion in a glucose\u2010dependent manner. Glucagon secretion is elevated with hypoglycemia but also with hyperglycemia. Within the pancreatic islet, \u03b1\u2010cell glucagon output is regulated by complex neuroendocrine and paracrine signals from insulin\u2010releasing \u03b2\u2010cells and somatostatin\u2010secreting \u03b4\u2010cells. This network of intra\u2010islet crosstalk tunes glucagon secretion in response to changes in glucose levels. In diabetes, intra\u2010islet paracrine crosstalk between \u2010, \u03b2\u2010, and \u03b4\u2010cells is disrupted. Autoimmune destruction of \u03b2\u2010cells or impaired \u03b1\u2010cell responsiveness to residual \u03b2\u2010cell signals leads to hyperglucagonemia. Conversely, the loss of controlled insulin secretion, along with elevated somatostatin levels, attenuates glucagon responses to hypoglycemia or to prolonged exercise. Antihypoglycemia therapies such as selective somatostatin receptor 2 antagonists have emerged as a novel strategy in managing iatrogenic insulin\u2010induced hypoglycemia. This review summarizes the latest experimental findings on the regulation of glucagon secretion by pancreatic \u03b2\u2010 and \u03b4\u2010cells, examines how this paracrine regulation of \u2010cell secretion is affected in diabetes, and highlights potential interventions aimed at restoring physiological glucagon dynamics.<\/jats:p>","DOI":"10.1111\/nyas.70384","type":"journal-article","created":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T11:47:54Z","timestamp":1789386474000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Intra\u2010Islet Paracrine Regulation of Glucagon Secretion During Hypoglycemia, Euglycemia, and Hyperglycemia"],"prefix":"10.1111","volume":"1563","author":[{"given":"Samaneh","family":"Fatehi","sequence":"first","affiliation":[{"name":"School of Kinesiology and Health Science York University  Toronto Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan V.","family":"Rocheleau","sequence":"additional","affiliation":[{"name":"UHN Research Institutes University Health Network  Toronto Ontario Canada"},{"name":"Institute of Biomedical Engineering University of Toronto  Toronto Ontario Canada"},{"name":"Departments of Medicine and Physiology University of Toronto  Toronto Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael C.","family":"Riddell","sequence":"additional","affiliation":[{"name":"School of Kinesiology and Health Science York University  Toronto Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,9,14]]},"reference":[{"key":"e_1_2_12_2_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00251826"},{"key":"e_1_2_12_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140\u20106736(75)92078\u20104"},{"key":"e_1_2_12_4_1","doi-asserted-by":"publisher","DOI":"10.3390\/s24030744"},{"key":"e_1_2_12_5_1","doi-asserted-by":"publisher","DOI":"10.1210\/clinem\/dgae626"},{"key":"e_1_2_12_6_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00492.2002"},{"key":"e_1_2_12_7_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00125\u2010019\u20104857\u20106"},{"key":"e_1_2_12_8_1","doi-asserted-by":"publisher","DOI":"10.1038\/s42255\u2010019\u20100158\u20100"},{"key":"e_1_2_12_9_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.00344.2014"},{"key":"e_1_2_12_10_1","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2012.00349"},{"key":"e_1_2_12_11_1","volume-title":"Endotext","author":"Davis H. 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