Abstract
Lipid metabolism in visceral fat cells is correlated with metabolic syndrome and cardiovascular diseases. Okadaic-acid, a 38-carbon fatty acid isolated from the black sponge Halichondria okadai, can stimulate lipolysis by promoting the phosphorylation of several proteins in adipocytes. However, the mechanism of okadaic acid-induced lipolysis and the effects of okadaic acid on lipid-droplet-associated proteins (perilipins and beta-actin) remain unclear. We isolated adipocytes from rat epididymal fat pads and treated them with isoproterenol and/or okadaic acid to estimate lipolysis by measuring glycerol release. Incubating adipocytes with okadaic acid stimulated time-dependent lipolysis. Lipid-droplet-associated perilipins and beta-actin were analyzed by immunoblotting and immunofluorescence, and the association of perilipin A and B was found to be decreased in response to isoproterenol or okadaic acid treatment. Moreover, okadaic-acid treatment could enhance isoproterenol-mediated lipolysis, whereas treatment of several inhibitors such as KT-5720 (PKA inhibitor), calphostin C (PKC inhibitor), or KT-5823 (PKG inhibitor) did not attenuate okadaic-acid-induced lipolysis. By contrast, vanadyl acetylacetonate (tyrosine phosphatase inhibitor) blocked okadaic-acid-dependent lipolysis. These results suggest that okadaic acid induces the phosphorylation and detachment of lipid-droplet-associated perilipin A and B from the lipid droplet surface and thereby leads to accelerated lipolysis.
Highlights
Adipose tissues play critical roles in energy storage, lipid metabolism, and glucose homeostasis
We investigated the effect of okadaic acid on lipolysis in rat visceral fat cells
Our results have demonstrated that treatment of adipocytes with okadaic acid can induce lipolysis in a time-dependent manner
Summary
Adipose tissues play critical roles in energy storage, lipid metabolism, and glucose homeostasis. The development of obesity may be due to excess adipose tissues accumulation or abnormal lipid metabolism. Obesity increases the risk of cardiovascular diseases and diabetes mellitus type 2, comorbidities often detected in metabolic syndrome [1], and visceral fat is linked to metabolic disorders and increased risk of cardiovascular disease [2, 3]. Many hormones and drugs have been identified to participate in the regulation of lipid metabolism, and various hormones and drugs lead to lipolysis through distinct lipolytic pathways [4]. The most studied lipolytic pathway is the cAMP-dependent protein kinase A (PKA) pathway in adipocytes, in which catecholamines bind to beta-adrenoreceptors and activate membrane-bound adenylyl cyclases and thereby increase intracellular cAMP formation [5].
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