Hayashi E, Maeda T, Hasegawa R, Tomita T
Biochim Biophys Acta. 1978 Nov 22;531(2):197-205. doi: 10.1016/0005-2760(78)90143-1.
myo-Inositol deficiency in rats produced an overaccumulation of triacylglycerols in the liver due to stimulated lipolysis in the adipose tissue (Hayashi, E., Maeda, T. and Tomita, T. (1974) Biochim. Biophys. Acta 360, 134--155). The mechanism of the enhancement in lipolysis has now been investigated. The lipolytic response to adrenalin, corticotropin and insulin of the epididymal adipose tissue did not change due to the deficiency, but hormone-sensitive lipase activity, plasma adrenalin level and blood pressure were higher in the deficient rats. Adrenalectomy had no influence, but administration of sympathetic nervous blockers (reserpine, hexamethonium and bupranolol) inhibited the liver lipid deposition and an increase of serum free fatty acids in the deficient rats. These results indicate that the enhancement in lipolysis is mediated by an excitation of sympathetic nerve terminals innervating in the adipose tissues.
大鼠体内的肌醇缺乏会导致肝脏中三酰甘油过度积累,这是由于脂肪组织中的脂肪分解受到刺激所致(林檎英、前田哲、富田敏夫,《生物化学与生物物理学学报》,1974年,第360卷,第134 - 155页)。目前已对脂肪分解增强的机制进行了研究。附睾脂肪组织对肾上腺素、促肾上腺皮质激素和胰岛素的脂解反应并未因缺乏肌醇而改变,但缺乏肌醇的大鼠体内激素敏感性脂肪酶活性、血浆肾上腺素水平和血压较高。肾上腺切除术没有影响,但给予交感神经阻滞剂(利血平、六甲铵和布普洛尔)可抑制缺乏肌醇的大鼠肝脏脂质沉积和血清游离脂肪酸增加。这些结果表明,脂肪分解的增强是由支配脂肪组织的交感神经末梢兴奋介导的。