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The underlying mechanisms are not well studied, and the effect of statin treatment on glucagon-like peptide 1 (GLP-1) secretion or production is unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>This work aimed to assess the effects of rosuvastatin on GLP-1 secretion and production.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We performed association studies in the Malm\u00f6 Diet and Cancer study cardiovascular cohort (MDCS-CC) reexamination cohort, in vitro investigations using GLUTag cells and acute and chronic studies in female, normoglycemic C57Bl\/6j mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Studies in the MDCS-CC reexamination cohort (n = 3734) revealed that in individuals without T2D, statin usage was associated with higher fasting glucose-dependent insulinotropic peptide (GIP), insulin, glucose, glucagon, and homeostatic model assessment of insulin resistance, but not GLP-1. However, in patients with T2D, statin usage was associated with higher fasting GLP-1 levels. Rosuvastatin treatment or 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (Hmgcr) knockdown (KD) reduced GLP-1 secretion and increased Gcg messenger RNA in GLUTag cells. Rosuvastatin acutely reduced postprandial GLP-1 secretion, whereas chronic rosuvastatin treatment in mice caused hyperglycemia and increased postprandial GLP-1 levels. The acute effect of Hmgcr KD on GLP-1 secretion could be mimicked by targeting intracellular cholesterol using a PCSK9 inhibitor. Finally, transcriptomic alterations induced by rosuvastatin were limited to genes involved in cholesterol biosynthesis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>We have established HMGCR as a regulator of GLP-1 secretion and provide a plausible explanation for the clinically observed mild hyperglycemia associated with statin use. Given the negative acute effect on GLP-1 secretion, monitoring of blood glucose levels is recommended after prescribing rosuvastatin.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1210\/clinem\/dgaf608","type":"journal-article","created":{"date-parts":[[2025,11,9]],"date-time":"2025-11-09T00:20:59Z","timestamp":1762647659000},"page":"e1343-e1355","source":"Crossref","is-referenced-by-count":1,"title":["HMGCR and Rosuvastatin Regulates GLP-1 Secretion and Expression\u2014A Translational Study"],"prefix":"10.1210","volume":"111","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4688-5719","authenticated-orcid":false,"given":"Michael G","family":"Miskelly","sequence":"first","affiliation":[{"name":"Neuroendocrine Cell Biology, Department of Experimental Medical Science, Lund University, Malm\u00f6 21428 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Lund 22100 ,","place":["Sweden"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6210-3142","authenticated-orcid":false,"given":"Maria F","family":"Gomez","sequence":"additional","affiliation":[{"name":"Diabetic Complications Unit, Department of Clinical Sciences, Lund University Diabetes Centre , Malm\u00f6 21428 ,","place":["Sweden"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6467-5029","authenticated-orcid":false,"given":"Lena","family":"Eliasson","sequence":"additional","affiliation":[{"name":"Islet Cell Exocytosis, Lund University Diabetes Centre, Lund University , Malm\u00f6 21428 ,","place":["Sweden"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6593-8417","authenticated-orcid":false,"given":"Hindrik","family":"Mulder","sequence":"additional","affiliation":[{"name":"Unit of Molecular Metabolism, Lund University Diabetes Centre , 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