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ludc web

Anna Wendt

Assistant researcher

ludc web

Dual Effect of Rosuvastatin on Glucose Homeostasis Through Improved Insulin Sensitivity and Reduced Insulin Secretion


  • Vishal A. Salunkhe
  • Ines Mollet
  • Jones K. Ofori
  • Helena A. Malm
  • Jonathan L S Esguerra
  • Thomas Reinbothe
  • Karin G. Stenkula
  • Anna Wendt
  • Lena Eliasson
  • Jenny Vikman

Summary, in English

Statins are beneficial in the treatment of cardiovascular disease (CVD), but these lipid-lowering drugs are associated with increased incidence of new on-set diabetes. The cellular mechanisms behind the development of diabetes by statins are elusive. Here we have treated mice on normal diet (ND) and high fat diet (HFD) with rosuvastatin. Under ND rosuvastatin lowered blood glucose through improved insulin sensitivity and increased glucose uptake in adipose tissue. In vitro rosuvastatin reduced insulin secretion and insulin content in islets. In the beta cell Ca2+ signaling was impaired and the density of granules at the plasma membrane was increased by rosuvastatin treatment. HFD mice developed insulin resistance and increased insulin secretion prior to administration of rosuvastatin. Treatment with rosuvastatin decreased the compensatory insulin secretion and increased glucose uptake. In conclusion, our data shows dual effects on glucose homeostasis by rosuvastatin where insulin sensitivity is improved, but beta cell function is impaired.


  • Diabetes - Islet Cell Exocytosis
  • Glucose Transport and Protein Trafficking
  • Genomics, Diabetes and Endocrinology
  • EXODIAB: Excellence of Diabetes Research in Sweden

Publishing year










Document type

Journal article




  • Pharmacology and Toxicology


  • Adipose tissue
  • Beta cell
  • Ca measurements
  • Glucose homeostasis
  • Glucose uptake
  • Insulin secretion
  • Islet
  • Muscle
  • OGTT
  • Statin
  • Transmission electron microscopy



Research group

  • Diabetes - Islet Cell Exocytosis
  • Glucose Transport and Protein Trafficking
  • Genomics, Diabetes and Endocrinology


  • ISSN: 2352-3964