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Insulin resistance and decreased glucose-stimulated insulin secretion after acute olanzapine administration

Araba F Chintoh1, Steve W Mann, Loretta Lam

  • 1Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada.

Journal of Clinical Psychopharmacology
|September 17, 2008
PubMed

Insights

Atypical antipsychotics like olanzapine can rapidly impair insulin secretion and sensitivity. This study reveals acute metabolic effects, including reduced glucose utilization and impaired beta-cell function, independent of weight gain.

Area of Science:

  • Pharmacology
  • Endocrinology
  • Metabolic Research

Background:

  • Atypical antipsychotics are linked to weight gain and metabolic issues.
  • The immediate mechanisms behind these metabolic changes are not fully understood.
  • This study investigates the acute impact of olanzapine on metabolic parameters.

Purpose of the Study:

  • To assess the acute effects of olanzapine on insulin sensitivity and secretion in healthy animals.
  • To determine if olanzapine causes rapid metabolic disturbances.
  • To investigate potential deficits in beta-cell functioning.

Main Methods:

  • Utilized hyperinsulinemic-euglycemic and hyperglycemic clamp techniques in animal models.
  • Administered olanzapine acutely (3 mg/kg sc) during clamp procedures.
  • Monitored glucose infusion rates, hepatic glucose production, glucose utilization, plasma insulin, and C-peptide levels.

Main Results:

  • Acute olanzapine administration decreased glucose infusion rates, indicating reduced insulin sensitivity.
  • Olanzapine increased hepatic glucose production and decreased peripheral glucose utilization.
  • Pretreatment with olanzapine led to hyperglycemia and significantly reduced insulin and C-peptide responses.

Conclusions:

  • Olanzapine induces rapid, direct metabolic changes affecting insulin sensitivity and secretion.
  • These acute effects occur before significant weight gain is expected.
  • Findings suggest olanzapine acutely impairs beta-cell function, contributing to metabolic abnormalities.

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