Cholecystokinin elevates mouse plasma lipids.

Cholecystokinin elevates mouse plasma lipids.
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DOI:
10.1371/journal.pone.0051011
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Guo Z
Guo Z
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Zhou L;Yang H;Lin X;Okoro EU;Guo Z

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胆囊收缩素(CCK)是一种肽类激素,可诱导胆汁释放到肠腔中,从而有助于脂肪在肠道中的消化和吸收。虽然胆汁酸和胆固醇排泄到粪便中可以消除体内的胆固醇,但本报告研究了CCK对小鼠血浆胆固醇和甘油三酯升高的影响。我们的数据表明,静脉注射50 ng/kg剂量的[Thr 28,Nle 31]-CCK使空腹低密度脂蛋白受体敲除(LDLR−/−)小鼠的血浆甘油三酯和胆固醇水平分别显著升高22%和31%。在野生型小鼠中,相同剂量的[Thr 28,Nle 31]-CCK分别诱导血浆甘油三酯和胆固醇增加6%和13%。然而,这些特定的CCK治疗前后的值没有达到统计学意义。口服橄榄油进一步升高血浆甘油三酯,但没有改变CCK治疗小鼠的血浆胆固醇水平。CCK处理小鼠血浆胆固醇增加分布在极低、低和高密度脂蛋白(VLDL、LDL和HDL)中,HDL增加较少。相应地,血浆载脂蛋白(apo)B48,B100,apoE和apoAI水平显着高于CCK治疗组小鼠比未治疗的对照组小鼠。胆管结扎、丙谷胺阻断CCK受体或依折麦布抑制尼曼-匹克C1样1转运蛋白可降低LDLR−/−小鼠中[Thr 28,Nle 31]-CCK的高胆固醇血症效应。这些结果表明,胆囊收缩素增加血浆胆固醇和甘油三酯作为一个结果的胆汁脂质从肠的重吸收。
Cholecystokinin (CCK) is a peptide hormone that induces bile release into the intestinal lumen which in turn aids in fat digestion and absorption in the intestine. While excretion of bile acids and cholesterol into the feces eliminates cholesterol from the body, this report examined the effect of CCK on increasing plasma cholesterol and triglycerides in mice. Our data demonstrated that intravenous injection of [Thr28, Nle31]-CCK at a dose of 50 ng/kg significantly increased plasma triglyceride and cholesterol levels by 22 and 31%, respectively, in fasting low-density lipoprotein receptor knockout (LDLR−/−) mice. The same dose of [Thr28, Nle31]-CCK induced 6 and 13% increases in plasma triglyceride and cholesterol, respectively, in wild-type mice. However, these particular before and after CCK treatment values did not achieve statistical significance. Oral feeding of olive oil further elevated plasma triglycerides, but did not alter plasma cholesterol levels in CCK-treated mice. The increased plasma cholesterol in CCK-treated mice was distributed in very-low, low and high density lipoproteins (VLDL, LDL and HDL) with less of an increase in HDL. Correspondingly, the plasma apolipoprotein (apo) B48, B100, apoE and apoAI levels were significantly higher in the CCK-treated mice than in untreated control mice. Ligation of the bile duct, blocking CCK receptors with proglumide or inhibition of Niemann-Pick C1 Like 1 transporter with ezetimibe reduced the hypercholesterolemic effect of [Thr28, Nle31]-CCK in LDLR−/− mice. These findings suggest that CCK-increased plasma cholesterol and triglycerides as a result of the reabsorption of biliary lipids from the intestine.
DOI: 10.1186/1743-7075-4-14
发表时间: 2007-06-05
影响因子: 4.5
作者:
Miyasaka, Kyoko;Kanai, Setsuko;Funakoshi, Akihiro
通讯作者: Funakoshi, Akihiro
DOI: 10.1074/jbc.m212377200
发表时间: 2003-04-11
影响因子: 4.8
作者:
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通讯作者: Attie, AD
DOI: 10.1161/atvbaha.108.179564
发表时间: 2009-04
期刊: Arteriosclerosis, thrombosis, and vascular biology
影响因子: --
作者:
Goldstein JL;Brown MS
通讯作者: Brown MS
DOI: 10.1128/mcb.23.21.7525-7530.2003
发表时间: 2003-11-01
影响因子: 5.3
作者:
Narisawa, S;Huang, L;Millán, JL
通讯作者: Millán, JL