Nitric Oxide and the Release of Lipoprotein Lipase from White Adipose Tissue

• Published in: Cellular physiology and biochemistry Vol. 22; no. 5-6; pp. 525 - 530
• Main Authors: Ricart-Jané, David, Casanovas, Albert, Jané, Núria, González, M.Alba, Buira-Morell, Irma, Ribera, Joan, Llobera, Miquel, López-Tejero, M. Dolores
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland Karger 01.01.2008
• Subjects: Adipose Tissue, White - cytology; Adipose Tissue, White - drug effects; Adipose Tissue, White - enzymology; Adipose Tissue, White - metabolism; Adipose tissues; Animals; Epididymis - enzymology; Immobilization; Lipase; Lipases; Lipoprotein Lipase - blood; Lipoprotein Lipase - metabolism; Lipoproteins; Lipoproteïnes; Male; Nitrates - blood; Nitric oxide; Nitric Oxide - metabolism; Nitric Oxide Donors - pharmacology; Nitric Oxide Synthase Type II - metabolism; Nitric Oxide Synthase Type III - metabolism; Original Paper; Perfusion; Peritoneum - enzymology; Rates (Animals de laboratori); Rats; Rats as laboratory animals; Rats, Wistar; Stress, Physiological - drug effects; Teixit adipós; Òxid nítric; Immobilization; Nitric oxide synthase; Acute stress; WAT perfusion; NO donor
• ISSN: 1015-8987; 1421-9778
• DOI: 10.1159/000185526

Background/Aim: Lipoprotein lipase (LPL) is the main enzyme responsible for the distribution of circulating triacylglycerides in tissues. Its regulation via release from active sites in the vascular endothelium is poorly understood. In a previous study we reported that in response to acute immobilization (IMMO), LPL activity rapidly increases in plasma and decreases in white adipose tissue (WAT) in rats. In other stress situations IMMO triggers a generalized increase in nitric oxide (NO) production. Methods/Results: Here we demonstrate that in rats: 1) in vivo acute IMMO rapidly increases NO concentrations in plasma 2) during acute IMMO the WAT probably produces NO via the endothelial isoform of nitric oxide synthase (eNOS) from vessels, and 3) epididymal WAT perfused in situ with an NO donor rapidly releases LPL from the endothelium. Conclusion: We propose the following chain of events: stress stimulus / rapid increase of NO production in WAT (by eNOS) / release of LPL from the endothelium in WAT vessels. This chain of events could be a new mechanism that promotes the rapid decrease of WAT LPL activity in response to a physiological stimulus.