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      Atrial natriuretic peptide contributes to physiological control of lipid mobilization in humans.

      The FASEB Journal

      Adipocytes, drug effects, metabolism, Adipose Tissue, Adrenergic alpha-Antagonists, pharmacology, Adrenergic beta-Antagonists, Adult, Atrial Natriuretic Factor, blood, physiology, secretion, Blood Glucose, analysis, Cross-Over Studies, Cyclic GMP, Double-Blind Method, Epinephrine, Exercise, Exercise Test, Extracellular Fluid, chemistry, Fatty Acids, Nonesterified, Glycerol, Guanylate Cyclase, Humans, Isoproterenol, Lipolysis, Male, Microdialysis, Norepinephrine, Oxygen Consumption, Phentolamine, Propanolamines, Propranolol, Receptors, Adrenergic, beta, Receptors, Atrial Natriuretic Factor, Subcutaneous Tissue, Sympathetic Nervous System, Thiophenes

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          Abstract

          In humans, lipid mobilization is considered to depend mainly on sympathetic nervous system activation and catecholamine action. A contribution of ANP was hypothesized because we have previously shown that atrial natriuretic peptide (ANP) is a lipolytic agent on isolated human fat cells. Control of lipid-mobilizing mechanisms was investigated using in situ microdialysis in subcutaneous adipose tissue (SCAT) in healthy young men during two successive exercise bouts performed at 35% and 60% peak oxygen consumption (VO2max) after placebo or acute oral tertatolol (nonselective beta-antagonist) treatment. In placebo-treated subjects, infusion of propranolol in the probe (100 micromol/l) only partially reduced (40%) the increment in extracellular glycerol concentration (EGC) promoted by exercise. Moreover, oral beta-adrenergic receptor blockade did not prevent exercise-induced lipid mobilization in SCAT while exerting fat cell beta-adrenergic receptor blockade. Exercise-induced increase in plasma ANP was potently amplified by oral tertatolol. A positive correlation was found between EGC and plasma ANP levels but also between extracellular cGMP (i.e., index of ANP-mediated lipolysis) and EGC. Thus, we demonstrate that exercise-induced lipid mobilization resistant to local propranolol and lipid-mobilizing action observed under oral beta-blockade is related to the action of ANP. Oral beta-adrenergic receptor blockade, which potentiates exercise-induced ANP release by the heart, may contribute to lipid mobilization in SCAT. The potential relevance of an ANP-related lipid-mobilizing pathway is discussed.

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          Journal
          15033935
          10.1096/fj.03-1086fje

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