LAUSR

Adiponectin is a white adipocyte hormone with insulin sensitizing properties. Correlations have been observed between adiponectin and different adipose tissue depots where serum adiponectin levels exhibit a negative relationship to visceral fat mass (VAT). Individuals with increased VAT have a greater risk for developing type 2 diabetes. We have previously shown that catecholamines stimulate acute adiponectin release from subcutaneous adipocytes via adrenergic beta-3-receptors (β 3 ARs) and Epac1. We further showed that this adrenergic stimulation was abolished in obesity/diabetes due to reduced levels of both β 3 ARs and Epac1. Here we aim to study the adrenergically stimulated adiponectin secretion in visceral adipocytes in health and in metabolic disease. Results obtained by ELISA revealed that epinephrine (EPI) and CL316243 (CL;β 3 AR-agonist) stimulated adiponectin release to a similar degree (∼2 fold) in primary visceral mouse adipocytes during 30 minutes incubation. The stimulatory effect of EPI was inhibited by Epac antagonist ESI-09 (P 3 AR as well as Epac1 in adipocytes isolated from control mice. In adipocytes isolated from obese/diabetic mice there was no change in expression of β 3 AR but an increase of Epac1 (P 3 AR and Epac1. It is an interesting finding that VAT adipocytes which are connected to several metabolically active organs largely maintain adrenergically stimulated adiponectin release in obesity/diabetes. Disclosure S. Musovic: None. S. Nguyen: None. C.S. Olofsson: None.