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 (β3ARs) and Epac1. We further showed that this adrenergic stimulation was abolished in obesity/diabetes due to reduced levels of both β3ARs 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;β3AR-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<0.05). Studies using visceral adipocytes isolated from obese/diabetic mice demonstrated that adiponectin release could still be stimulated with EPI and CL (∼1.5 fold) although at a significantly lower magnitude compared to control mice (P<0.001). RT-qPCR results showed a high expression of β3AR as well as Epac1 in adipocytes isolated from control mice. In adipocytes isolated from obese/diabetic mice there was no change in expression of β3AR but an increase of Epac1 (P<0.001). Our results propose that acute adiponectin release in visceral adipocytes is regulated through activation of β3AR 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.
S. Musovic: None. S. Nguyen: None. C.S. Olofsson: None.