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腹内侧下丘脑损伤雄性大鼠的摄食过量及饮食组成对代谢的影响

The significance of hyperphagia and diet composition on the metabolism in ventromedial hypothalamic lesioned male rats.

作者信息

Hansen F M, Nilsson P, Hustvedt B E, Nilsson-Ehle P, Løvø A

出版信息

Horm Metab Res. 1983 Nov;15(11):538-42. doi: 10.1055/s-2007-1018782.

Abstract

The metabolic consequences of ventromedial hypothalamic lesion were studied in a group of aged male rats which were obese and had decreased response to insulin. The effects of hyperphagia and ventromedial hypothalamic lesion per se were separated by comparing experimental animals fed isocalorically with controls and animals fed ad libitum. Ventromedial hypothalamic lesion as such led to increases in the glucose conversion to fatty acid and in lipoprotein lipase activity in adipose tissue. Protein catabolism as reflected by plasma urea levels, was enhanced. The lipoprotein lipase activity in heart tended to be lower after VMH lesion. These metabolic changes were amplified in the VMH lesioned rats fed ad libitum. The liver glycogen content was lowered by VMH lesion, but this effect was abolished by hyperphagia. In parallel experiments the influence of diet composition was studied by feeding similar groups with diet of high fat content. The glucose incorporation in fatty acids was in all groups markedly and similarly inhibited by the high fat diet. The increase in lipoprotein lipase activity in heart and adipose tissue of control rats with high fat intake could not be demonstrated in any of the groups with ventromedial hypothalamic lesion. The plasma urea level in the control group was not affected by the diet, but tended to increase in the ventromedial hypothalamic lesioned groups on high fat intake. These findings demonstrate that the well known metabolic effects of ventromedial hypothalamic lesions are also manifest in obese insulin resistant male rats. Furthermore, the responses to changes in diet composition are different from those of the control rats.

摘要

在一组肥胖且对胰岛素反应降低的老年雄性大鼠中,研究了腹内侧下丘脑损伤的代谢后果。通过将等热量喂养的实验动物与对照组以及自由进食的动物进行比较,分离出了摄食过多和腹内侧下丘脑损伤本身的影响。腹内侧下丘脑损伤本身导致葡萄糖向脂肪酸的转化率以及脂肪组织中脂蛋白脂肪酶活性增加。血浆尿素水平所反映的蛋白质分解代谢增强。腹内侧下丘脑损伤后,心脏中的脂蛋白脂肪酶活性趋于降低。在自由进食的腹内侧下丘脑损伤大鼠中,这些代谢变化被放大。腹内侧下丘脑损伤会降低肝脏糖原含量,但这种影响会因摄食过多而消除。在平行实验中,通过给类似的组喂食高脂肪含量的饮食来研究饮食组成的影响。高脂肪饮食在所有组中均显著且相似地抑制了葡萄糖掺入脂肪酸的过程。在任何腹内侧下丘脑损伤的组中,均未观察到高脂肪摄入的对照大鼠心脏和脂肪组织中脂蛋白脂肪酶活性的增加。对照组的血浆尿素水平不受饮食影响,但在高脂肪摄入的腹内侧下丘脑损伤组中趋于升高。这些发现表明,腹内侧下丘脑损伤的众所周知的代谢效应在肥胖的胰岛素抵抗雄性大鼠中也很明显。此外,对饮食组成变化的反应与对照大鼠不同。

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