Endocrine Abstracts

Background and aims: Adiponectin produced by visceral adipocytes is believed to be marker of insulin sensitivity. Glitazones (PPARγ agonists) induce adipocetin transcription and secretion. β3 agonists are potencial antiobesity drugs with lipolytic activity. We try to shed light on the relationship between PPARγ, β3 signaling, and adiponectin secretion.

Methods: Epididymal rat adipocytes were isolated and cultivated together with troglitazone (PPARγ agonist), BRL-37344 (β3 agonist) alone and in combinations. After 1, 2, 12, 24, 48, 72 h, culture media were analyzed via ELISA for adiponectin level.

Results: Adiponectin reacted as expected to glitazone addition (adiponectin increased, resistin decreased) after more than 24 h incubation. However, adiponectin level was paradoxically decreased after 24 h but increased more than control after 48 h. Interestingly BRL-37344 produced remarkable increase of adiponectin in 1 h of cultivation with subsequent decrease to control level in 2 h. That means β3 agonist could enhance secretion of adiponectin as a very soon response. The adiponectin level under PPARγ agonist treatment remains in control level in first 2 h. The two substances did not show significant interactions mediating adiponectin secretion.

Conclusions: The time dependence of adiponectin secretion in response to Troglitazone is demonstrated. β3 agonist effect on adiponectin secretion in visceral rat adipocytes is described. The secretion of adiponectin is not modulated by PPARγ+β3 interactions. Supported by VZ MSM 0021620807.