Atrial natriuretic peptide contributes to physiological control of lipid mobilization in humans.
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.
Moro
Cedric
C
Unité de recherches sur les Obésités, Institut National de la Santé et de la Recherche Médicale U586 ,Toulouse, France.
Crampes
Francois
F
Sengenes
Coralie
C
De Glisezinski
Isabelle
I
Galitzky
Jean
J
Thalamas
Claire
C
Lafontan
Max
M
Berlan
Michel
M
D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism; D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism*; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000328:Adult; D009320:Atrial Natriuretic Factor / Q000097:blood / Q000378:metabolism / Q000502:physiology*; D001786:Blood Glucose / Q000032:analysis; D018592:Cross-Over Studies; D006152:Cyclic GMP / Q000378:metabolism; D004311:Double-Blind Method; D004837:Epinephrine / Q000097:blood; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D045604:Extracellular Fluid / Q000737:chemistry; D005230:Fatty Acids, Nonesterified / Q000032:analysis / Q000097:blood; D005990:Glycerol / Q000032:analysis / Q000097:blood; D006162:Guanylate Cyclase / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D008066:Lipolysis / Q000187:drug effects / Q000502:physiology*; D008297:Male; D017551:Microdialysis; D009638:Norepinephrine / Q000097:blood; D010101:Oxygen Consumption; D010646:Phentolamine / Q000494:pharmacology; D011412:Propanolamines / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000502:physiology; D017461:Receptors, Atrial Natriuretic Factor / Q000187:drug effects / Q000502:physiology; D040521:Subcutaneous Tissue / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000502:physiology; D013876:Thiophenes / Q000494:pharmacology
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D011412:Propanolamines; D011943:Receptors, Adrenergic, beta; D013876:Thiophenes; D009320:Atrial Natriuretic Factor; D011433:Propranolol; C005632:tertatolol; D006162:Guanylate Cyclase; D017461:Receptors, Atrial Natriuretic Factor; C091715:atrial natriuretic factor receptor A; D006152:Cyclic GMP; D007545:Isoproterenol; D005990:Glycerol; D009638:Norepinephrine; D004837:Epinephrine; D010646:Phentolamine