Suppr超能文献

阿托伐他汀增加蔗糖喂养大鼠的肝脏脂肪酸β-氧化:与一种微粒体甘油三酯转运蛋白抑制剂的比较。

Atorvastatin increases hepatic fatty acid beta-oxidation in sucrose-fed rats: comparison with an MTP inhibitor.

作者信息

Funatsu Toshiyuki, Kakuta Hirotoshi, Takasu Toshiyuki, Miyata Keiji

机构信息

Pharmacology Laboratories, Institute for Drug Discovery Research, Yamanouchi Pharmaceutical Co, Ltd, 21 Miyukigaoka, Tsukuba, Ibaraki 3058585, Japan.

出版信息

Eur J Pharmacol. 2002 Nov 29;455(2-3):161-7. doi: 10.1016/s0014-2999(02)02611-0.

Abstract

We investigated the effects of atorvastatin, a widely used 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, and BMS-201038, a microsomal triglyceride transfer protein (MTP) inhibitor, in sucrose-fed hypertriglyceridemic rats to determine whether the activation of beta-oxidation by these compounds plays a role in their hypotriglyceridemic effect. The decrease in plasma triglyceride concentration and post-Triton very low-density lipoprotein (VLDL) triglyceride concentration, a measure of hepatic triglyceride secretion, by atorvastatin (30 mg/kg p.o.) for 2 weeks was to approximately the same degree as those by BMS-201038 (0.3 mg/kg). Atorvastatin (30 mg/kg) increased hepatic beta-oxidation activity by 54% (P < 0.01), while BMS-201038 (0.3 mg/kg) had no significant effect. Atorvastatin decreased hepatic triglyceride, fatty acid and cholesteryl ester concentrations by 21% to 39%, whereas BMS-201038 increased these variables by 28% to 307%. In the atorvastatin-treated groups, a significant relationship was seen not only between hepatic beta-oxidation activity and hepatic triglyceride concentration (R(2) = 0.535, P < 0.01), but also between hepatic and plasma triglyceride concentrations (R(2) = 0.586, P < 0.01). No effect of atorvastatin on hepatic fatty acid synthesis was observed. These results indicate that the activation of hepatic beta-oxidation by atorvastatin may contribute to the decrease in hepatic triglyceride concentration, leading to its hypotriglyceridemic effect.

摘要

我们研究了广泛使用的3-羟基-3-甲基戊二酰辅酶A(HMG-CoA)还原酶抑制剂阿托伐他汀和微粒体甘油三酯转移蛋白(MTP)抑制剂BMS-201038对蔗糖喂养的高甘油三酯血症大鼠的影响,以确定这些化合物激活β-氧化是否在其降甘油三酯作用中起作用。阿托伐他汀(30mg/kg口服)连续2周使血浆甘油三酯浓度和经曲拉通处理后的极低密度脂蛋白(VLDL)甘油三酯浓度(衡量肝脏甘油三酯分泌的指标)降低的程度,与BMS-201038(0.3mg/kg)大致相同。阿托伐他汀(30mg/kg)使肝脏β-氧化活性增加了54%(P<0.01),而BMS-201038(0.3mg/kg)没有显著影响。阿托伐他汀使肝脏甘油三酯、脂肪酸和胆固醇酯浓度降低了21%至39%,而BMS-201038使这些变量增加了28%至307%。在阿托伐他汀治疗组中,不仅肝脏β-氧化活性与肝脏甘油三酯浓度之间存在显著相关性(R²=0.535,P<0.01),而且肝脏与血浆甘油三酯浓度之间也存在显著相关性(R²=0.586,P<0.01)。未观察到阿托伐他汀对肝脏脂肪酸合成有影响。这些结果表明,阿托伐他汀激活肝脏β-氧化可能有助于降低肝脏甘油三酯浓度,从而产生其降甘油三酯作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验