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高肝素后脂解活性作为自发性高血压大鼠低甘油三酯血症的可能原因。

High postheparin lipolytic activity as a possible cause of hypotriglyceridemia in spontaneously hypertensive rats.

作者信息

Singer P, Berger I, Moritz V, Baumann R

出版信息

Acta Biol Med Ger. 1980;39(7):819-24.

PMID:7211069
Abstract

In male spontaneously hypertensive rats (SHR) and normotensive Wistar rats at 4, 8 and 20 weeks of age the postheparin lipolytic activity (PHLA) has been estimated. PHLA was significantly higher in all SHR than in age- and weight-matched controls, although it decreased with advancing age in both groups. The data are discussed with regard to hyperinsulinemia and hypotriglyceridemia in SHR ascertained by a previous study. It is assumed that in young SHR catecholamine-induced lipolysis provokes impaired glucose tolerance and higher insulin response after glucose load. Insulin enhancement can stimulate PHLA via increased synthesis of lipoprotein lipase. The resulting augmented uptake of triglycerides by adipose tissue is suggested to be a beneficial (adaptive?) mechanism to compensate a primary increase of lipolysis. The well-known lower adipose cell size and body weight in SHR in comparison to age-related normotensive control rats might indicate that this mechanism is insufficient to balance the triglyceride supply in these animals.

摘要

在4周、8周和20周龄的雄性自发性高血压大鼠(SHR)和正常血压的Wistar大鼠中,对肝素后脂解活性(PHLA)进行了评估。所有SHR的PHLA均显著高于年龄和体重匹配的对照组,尽管两组中PHLA均随年龄增长而降低。结合先前一项研究所确定的SHR中的高胰岛素血症和低甘油三酯血症对这些数据进行了讨论。据推测,在年轻的SHR中,儿茶酚胺诱导的脂解会引发葡萄糖耐量受损以及葡萄糖负荷后更高的胰岛素反应。胰岛素增加可通过增加脂蛋白脂肪酶的合成来刺激PHLA。由此导致脂肪组织对甘油三酯摄取增加,这被认为是一种有益的(适应性的?)机制,以补偿脂解的原发性增加。与年龄相关的正常血压对照大鼠相比,SHR中众所周知的较小脂肪细胞大小和体重可能表明这种机制不足以平衡这些动物的甘油三酯供应。

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