Minokoshi Y, Saito M, Shimazu T
Department of Medical Biochemistry, School of Medicine, Ehime University, Japan.
Neurosci Lett. 1990 Feb 16;109(3):341-6. doi: 10.1016/0304-3940(90)90019-6.
Intermittent electrical stimulation of sympathetic nerves entering the interscapular brown adipose tissue (BAT) in rats increased the rate of glyceride glycerol synthesis in BAT but the fatty acid synthesis did not change. Simultaneous administration of phenoxybenzamine and propranolol paradoxically increased the fatty acid synthesis in response to the nerve stimulation whereas the glyceride glycerol synthesis was inhibited. Propranolol alone was also effective in mimicking the effects of adrenergic blockade, but guanethidine selectively eliminated the lipogenic response to the nerve stimulation. These results indicate that synthesis of glyceride glycerol induced by sympathetic nerve stimulation is largely due to beta-adrenergic action of noradrenaline, whereas synthesis of fatty acids may be mediated by non-adrenergic transmission of the sympathetic nerves.
间歇性电刺激进入大鼠肩胛间棕色脂肪组织(BAT)的交感神经,会提高BAT中甘油甘油酯的合成速率,但脂肪酸合成并未改变。同时给予苯氧苄胺和普萘洛尔,反而会增加神经刺激引起的脂肪酸合成,而甘油甘油酯的合成则受到抑制。单独使用普萘洛尔也能有效模拟肾上腺素能阻断的效果,但胍乙啶能选择性消除对神经刺激的脂肪生成反应。这些结果表明,交感神经刺激诱导的甘油甘油酯合成主要归因于去甲肾上腺素的β-肾上腺素能作用,而脂肪酸合成可能由交感神经的非肾上腺素能传递介导。