Fluvastatin Reduces Glucose Tolerance in Healthy Young Individuals Independently of Cold Induced BAT Activity

Martina Felder1, Claudia Irene Maushart1, Gani Gashi1

  • 1Department of Endocrinology, Diabetes and Metabolism, University Hospital Basel and University of Basel, Basel, Switzerland.

Insights

Statin use, like fluvastatin, can impair glucose tolerance by increasing glucose levels, even while lowering cholesterol. This study suggests statins may affect glucose metabolism independently of brown adipose tissue (BAT) activity.

Area of Science:

  • Endocrinology
  • Metabolic Syndrome
  • Pharmacology

Background:

  • Statins are widely used for cardiovascular disease prevention by inhibiting HMG-CoA-reductase.
  • Emerging evidence links statin use to an increased risk of diabetes mellitus.
  • The underlying mechanisms, potentially involving brown adipose tissue (BAT) and insulin resistance, are not fully understood.

Purpose of the Study:

  • To investigate the impact of fluvastatin on glucose tolerance and BAT activity in healthy men.
  • To explore the potential role of BAT inhibition in statin-induced insulin resistance.

Main Methods:

  • A prospective study involving 17 healthy men.
  • Assessment of cold-induced thermogenesis (CIT) and BAT activity using FDG-PET/MRI.
  • Oral glucose tolerance tests (oGTT) and lipid profiles before and after two weeks of fluvastatin treatment.

Main Results:

  • Fluvastatin significantly increased glucose area under the curve (AUC) during oGTT, indicating reduced glucose tolerance.
  • Total and LDL cholesterol levels were significantly reduced.
  • No significant changes were observed in insulin AUC, resting energy expenditure, diet-induced thermogenesis, or BAT activity parameters (SUVmean, volume, glycolysis).

Conclusions:

  • Two weeks of fluvastatin treatment in healthy men impaired glucose tolerance without affecting cold-induced BAT activity.
  • The findings suggest that statins may negatively impact glucose metabolism through mechanisms other than direct inhibition of BAT activity.
Abstract

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