Moro Cedric, Crampes Francois, Sengenes Coralie, De Glisezinski Isabelle, Galitzky Jean, Thalamas Claire, Lafontan Max, Berlan Michel
Unité de recherches sur les Obésités, Institut National de la Santé et de la Recherche Médicale U586 ,Toulouse, France.
FASEB J. 2004 May;18(7):908-10. doi: 10.1096/fj.03-1086fje. Epub 2004 Mar 19.
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.
在人类中，脂质动员被认为主要依赖于交感神经系统的激活和儿茶酚胺的作用。由于我们之前已经表明心房利钠肽（ANP）是分离的人类脂肪细胞上的一种脂解剂，因此推测ANP也有作用。在健康年轻男性中，通过在皮下脂肪组织（SCAT）中进行原位微透析，研究了在安慰剂或急性口服酒石酸美托洛尔（非选择性β受体拮抗剂）治疗后，在两次连续运动期间，以35%和60%的峰值耗氧量（VO2max）进行运动时脂质动员机制的控制情况。在接受安慰剂治疗的受试者中，向探针中注入普萘洛尔（100微摩尔/升）仅部分降低了（40%）运动促进的细胞外甘油浓度（EGC）的增加。此外，口服β肾上腺素能受体阻滞剂在对脂肪细胞β肾上腺素能受体进行阻滞的同时，并未阻止运动诱导的SCAT中的脂质动员。口服酒石酸美托洛尔可有效放大运动诱导的血浆ANP升高。发现EGC与血浆ANP水平之间存在正相关，但细胞外cGMP（即ANP介导的脂解指标）与EGC之间也存在正相关。因此我们证明，运动诱导的对局部普萘洛尔有抗性的脂质动员以及在口服β受体阻滞剂情况下观察到的脂质动员作用与ANP的作用有关。口服β肾上腺素能受体阻滞剂可增强心脏运动诱导的ANP释放，可能有助于SCAT中的脂质动员。本文讨论了与ANP相关的脂质动员途径的潜在相关性。
