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White Adipocyte Adiponectin Exocytosis Is Stimulated via beta(3)-Adrenergic Signaling and Activation of Epac1: Catecholamine Resistance in Obesity and Type 2 Diabetes

Artikel i vetenskaplig tidskrift
Författare Ali Komai
Musovic Saliha
Eduard Peris
Ahmed Alrifaiy
Michael El Hachmane
Marcus Johansson
Ingrid Wernstedt Asterholm
Charlotta S Olofsson
Publicerad i Diabetes
Volym 65
Nummer/häfte 11
Sidor 3301-3313
ISSN 0012-1797
Publiceringsår 2016
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Sidor 3301-3313
Språk en
Länkar dx.doi.org/10.2337/db15-1597
Ämnesord beta-adrenoceptor agonists, 3t3-l1 adipocytes, fat-cells, insulin-secretion, calcium-channels, ca2+ regulation, expression, protein, organization, microdomains, Endocrinology & Metabolism
Ämneskategorier Endokrinologi

Sammanfattning

We investigated the physiological regulation of adiponectin exocytosis in health and metabolic disease by a combination of membrane capacitance patch-clamp recordings and biochemical measurements of short-term (30-min incubations) adiponectin secretion. Epinephrine or the beta(3)-adrenergic receptor (AR) agonist CL 316,243 (CL) stimulated adiponectin exocytosis/secretion in cultured 3T3-L1 and in primary subcutaneous mouse adipocytes, and the stimulation was inhibited by the Epac (Exchange Protein directly Activated by cAMP) antagonist ESI-09. The beta(3)AR was highly expressed in cultured and primary adipocytes, whereas other ARs were detected at lower levels. 3T3-L1 and primary adipocytes expressed Epac1, whereas Epac2 was undetectable. Adiponectin secretion could not be stimulated by epinephrine or CL in adipocytes isolated from obese/type 2 diabetic mice, whereas the basal (unstimulated) adiponectin release level was elevated twofold. Gene expression of beta(3)AR and Epac1 was reduced in adipocytes from obese animals, and corresponded to a respective similar to 35% and similar to 30% reduction at the protein level. Small interfering RNA-mediated knockdown of beta(3)AR (similar to 60%) and Epac1 (similar to 50%) was associated with abrogated catecholamine-stimulated adiponectin secretion. We propose that adiponectin exocytosis is stimulated via adrenergic signaling pathways mainly involving beta(3)ARs. We further suggest that adrenergically stimulated adiponectin secretion is disturbed in obesity/type 2 diabetes as a result of the reduced expression of beta(3)ARs and Epac1 in a state we define as "catecholamine resistance."

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