Fluid Retention With Rosiglitazone Not Tied to Vascular Tone

Fluid retention, the investigators conclude, is not caused by improvement of the vascular actions of insulin.

Studies in obese, insulin-resistant non-diabetic subjects do not support the hypothesis that the fluid retention associated with thiazolidinedione derivatives such as rosiglitazone is directly due to vascular tone or permeability, Dutch and UK researchers report..

Lead investigator Dr. Alexander J. M. Rennings, stated that, “These agents generally induce some increase in plasma volume, while the susceptibility to develop edema seems to be dependent on individual characteristics, like, for example, improvement in insulin sensitivity."

"However," he added, "we have to be careful about extrapolating the result of this mechanistic study in a non-diabetic population to patients with diabetes."

To avoid the confounding effects of improved glycemic control, Dr. Rennings of Radboud University Nijmegan Medical Center and colleagues studied 18 obese, non-diabetic subjects with characteristics of the metabolic syndrome. In a double-blind crossover study, they were randomized to 4 mg of rosiglitazone or placebo twice daily for 12 weeks.

Rosiglitazone increased the glucose infusion rate during hyperinsulinemic-euglycemic clamping. Overall, there was a correlation between glucose disposal and change in foot volume. However, there was no effect on vascular permeability or blood flow response to hyperinsulinemia.

Rosiglitazone decreased diastolic blood pressure and appeared to reduce calculated systemic vascular resistance, but this did not reach statistical significance.

Rosiglitazone did increase plasma volume and one subject developed edema and a 4.6% increase in foot volume.
Fluid retention, the investigators conclude, is not caused by improvement of the vascular actions of insulin. Nevertheless, they add, "rosiglitazone-induced improvement in insulin sensitivity appears to be correlated to edema formation."
Diabetes Care 2006;29:581-587.

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