de Glisezinski I, Larrouy D, Bajzova M, Koppo K, Polak J, Berlan M, Bulow J, Langin D, Marques M A, Crampes F, Lafontan M, Stich V
Institut National de la Santé et de la Recherche Médicale, Toulouse, France.
J Physiol. 2009 Jul 1;587(Pt 13):3393-404. doi: 10.1113/jphysiol.2009.168906. Epub 2009 May 5.
The relative contribution of noradrenaline (norepinephrine) and adrenaline (epinephrine) in the control of lipid mobilization in subcutaneous adipose tissue (SCAT) during exercise was evaluated in men treated with a somatostatin analogue, octreotide. Eight lean and eight obese young men matched for age and physical fitness performed 60 min exercise bouts at 50% of their maximal oxygen consumption on two occasions: (1) during i.v. infusion of octreotide, and (2) during placebo infusion. Lipolysis and local blood flow changes in SCAT were evaluated using in situ microdialysis. Infusion of octreotide suppressed plasma insulin and growth hormone levels at rest and during exercise. It blocked the exercise-induced increase in plasma adrenaline while that of noradrenaline was unchanged. Plasma natriuretic peptides (NPs) level was higher at rest and during exercise under octreotide infusion in lean men. Under placebo, no difference was found in the exercise-induced increase in glycerol between the probe perfused with Ringer solution alone and that with phentolamine (an alpha-adrenergic receptor antagonist) in lean subjects while a greater increase in glycerol was observed in the obese subjects. Under placebo, propranolol infusion in the probe containing phentolamine reduced by about 45% exercise-induced glycerol release; this effect was fully suppressed under octreotide infusion while noradrenaline was still elevated and exercise-induced lipid mobilization maintained in both lean and obese individuals. In conclusion, blockade of beta-adrenergic receptors during exercise performed during infusion of octreotide (blocking the exercise-induced rise in adrenaline but not that of noradrenaline) does not alter the exercise-induced lipolysis. This suggests that adrenaline is the main adrenergic agent contributing to exercise-induced lipolysis in SCAT. Moreover, it is the combined action of insulin suppression and NPs release which explains the lipolytic response which remains under octreotide after full local blockade of fat cell adrenergic receptors. For the moment, it is unknown if results apply specifically to SCAT and exercise only or if conclusions could be extended to all forms of lipolysis in humans.
在接受生长抑素类似物奥曲肽治疗的男性中,评估了去甲肾上腺素和肾上腺素在运动过程中对皮下脂肪组织(SCAT)脂质动员控制中的相对贡献。八名年龄和体能相匹配的瘦年轻男性和八名肥胖年轻男性分两次进行了60分钟的运动,运动强度为其最大耗氧量的50%:(1)静脉输注奥曲肽期间;(2)安慰剂输注期间。使用原位微透析评估SCAT中的脂肪分解和局部血流变化。输注奥曲肽可抑制静息和运动期间的血浆胰岛素和生长激素水平。它阻断了运动诱导的血浆肾上腺素升高,而去甲肾上腺素水平不变。在瘦男性中,输注奥曲肽时静息和运动期间血浆利钠肽(NPs)水平较高。在安慰剂条件下,瘦受试者中仅用林格溶液灌注的探针与用酚妥拉明(一种α-肾上腺素能受体拮抗剂)灌注的探针之间,运动诱导的甘油增加无差异,而肥胖受试者中甘油增加更大。在安慰剂条件下,在含有酚妥拉明的探针中输注普萘洛尔可使运动诱导的甘油释放减少约45%;在输注奥曲肽时这种作用被完全抑制,但去甲肾上腺素仍升高,且运动诱导的脂质动员在瘦和肥胖个体中均得以维持。总之,在输注奥曲肽期间进行运动时阻断β-肾上腺素能受体(阻断运动诱导的肾上腺素升高但不阻断去甲肾上腺素升高)不会改变运动诱导的脂肪分解。这表明肾上腺素是导致SCAT中运动诱导脂肪分解的主要肾上腺素能介质。此外,可以解释在脂肪细胞肾上腺素能受体完全局部阻断后奥曲肽作用下仍存在的脂肪分解反应的是胰岛素抑制和NPs释放两者的联合作用。目前尚不清楚这些结果是否仅特别适用于SCAT和运动情况,还是这些结论可以扩展到人类所有形式的脂肪分解情况。