Atrial natriuretic peptide contributes to the physiological control of lipid mobilization in humans
Atrial natriuretic peptide contributes to the physiological control of lipid mobilization in humans
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DOI：
10.1096/fj.03-1086fje
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发表时间：
2004-03-01
期刊：
影响因子：
4.8
通讯作者：
Berlan, M
中科院分区：
文献类型：
--
作者：
Moro, C;Crampes, F;Berlan, M
在人类中，脂质动员被认为主要取决于交感神经系统的激活和儿茶酚胺的作用。假设 ANP 的贡献是因为我们之前已经证明心房钠尿肽 (ANP) 是分离的人体脂肪细胞的脂肪分解剂。在安慰剂或急性口服特他洛尔（非选择性 β 拮抗剂）治疗后，在 35% 和 60% 峰值耗氧量 (VO(2)max) 下进行的两次连续运动中，使用皮下脂肪组织原位微透析 (SCAT) 来研究脂质动员机制的控制。在安慰剂治疗的受试者中，在探针中输注普萘洛尔（100μmol/l）仅部分减少（40%）运动引起的细胞外甘油浓度（EGC）的增加。此外，口服β-肾上腺素能受体阻断剂在发挥脂肪细胞β-肾上腺素能受体阻断作用时，并不能阻止运动诱导的SCAT脂质动员。口服特他洛尔可有效放大运动引起的血浆 ANP 增加。我们发现 EGC 和血浆 ANP 水平之间存在正相关，而且细胞外 cGMP（即 ANP 介导的脂肪分解指数）和 EGC 之间也存在正相关。因此，我们证明运动诱导的脂质动员对局部普萘洛尔有抵抗力，并且在口服β-阻滞剂下观察到的脂质动员作用与ANP的作用有关。口服β-肾上腺素能受体阻断剂可增强运动引起的心脏 ANP 释放，可能有助于 SCAT 中的脂质动员。讨论了 ANP 相关脂质动员途径的潜在相关性。
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 (VO(2)max) after placebo or acute oral tertatolol (nonselective beta-antagonist) treatment. In placebo-treated subjects, infusion of propranolol in the probe (100 mumol/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.