HMGCR and Rosuvastatin Regulates GLP-1 Secretion and Expression—A Translational Study
Authors' conclusion
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.
Study context
- Population
- Malmö Diet and Cancer study cardiovascular cohort (MDCS-CC) reexamination cohort; GLUTag cells; female normoglycemic C57Bl/6j miceMDCS-CC reexamination cohort
- Participants
- 3,734 participants
- Comparison
- Statin use vs no statin use; rosuvastatin or Hmgcr knockdown (KD) vs control
- Outcome
- Effects of rosuvastatin on GLP-1 secretion and production
Methodological detailscohort association study, in vitro GLUTag cells, acute and chronic mouse studies
- Cohort association study
- In vitro GLUTag cells
- Acute and chronic mouse studies
Main finding
As reported in the abstract
- Without T2D, statin use associated with higher fasting GIP, insulin, glucose, glucagon and HOMA-IR, but not GLP-1
- In T2D, statin use associated with higher fasting GLP-1
- Rosuvastatin or Hmgcr KD reduced GLP-1 secretion and increased Gcg mRNA in GLUTag cells
- Rosuvastatin acutely reduced postprandial GLP-1 secretion
- Chronic rosuvastatin in mice caused hyperglycemia and increased postprandial GLP-1
- Acute effect of Hmgcr KD on GLP-1 secretion mimicked by a PCSK9 inhibitor targeting intracellular cholesterol
- Rosuvastatin-induced transcriptomic alterations limited to cholesterol biosynthesis genes
Original publication
HMGCR and Rosuvastatin Regulates GLP-1 Secretion and Expression—A Translational Study. J Clin Endocrinol Metab. Published 5 November 2025. doi:10.
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