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Interactions of doxazosin with insulin or glucagon in the ob/ob mouse

A C Swindell1, J J Valentine

  • 1Central Research Division, Pfizer Inc., Groton, Connecticut 06340.

Insights

Doxazosin, an alpha 1-adrenergic receptor inhibitor, impacts lipid and glucose metabolism in mice. It lowers triglycerides and cholesterol, suggesting a role in glycemic control and lipid regulation, especially with insulin resistance.

Area of Science:

  • Pharmacology
  • Endocrinology
  • Metabolic Research

Background:

  • Obese (ob/ob) mice exhibit insulin resistance and metabolic dysregulation.
  • Alpha 1-adrenergic receptors play a role in various physiological processes, including cardiovascular and metabolic functions.

Purpose of the Study:

  • To investigate the effects of doxazosin, a selective alpha 1-adrenergic receptor inhibitor, on lipid and glucose metabolism in ob/ob mice.
  • To explore the interactions between doxazosin, insulin, and glucagon on metabolic parameters.

Main Methods:

  • Administration of doxazosin alone or in combination with insulin or glucagon to mature ob/ob mice.
  • Measurement of serum levels of triglycerides, cholesterol, glycerol, lactate, beta-hydroxybutyrate, glucose, and free fatty acids (FFA).
  • Statistical analysis using analysis of variance to assess interactions between treatments.

Main Results:

  • Doxazosin consistently lowered triglycerides, cholesterol, glycerol, and lactate, while increasing beta-hydroxybutyrate and glucose.
  • Doxazosin modulated insulin's effect on triglycerides but not on hypoglycemia.
  • Combined administration of doxazosin and insulin, but not alone, reduced FFA.
  • Glucagon affected cholesterol and glucose but not triglycerides or beta-hydroxybutyrate.
  • Interactions between doxazosin and insulin on triglycerides, glucose, and FFA could not be explained by simple additive effects.

Conclusions:

  • The alpha 1-adrenergic system may contribute to glycemic control and hypercholesterolemia, particularly in insulin-resistant states like that seen in ob/ob mice.
  • The hypolipidemic effects of alpha 1-adrenergic inhibition might involve insulin-dependent pathways.

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