Modulation of sphingosine-1-phosphate and apolipoprotein M levels in the plasma, liver and kidneys in streptozotocin-induced diabetic mice.

Modulation of sphingosine-1-phosphate and apolipoprotein M levels in the plasma, liver and kidneys in streptozotocin-induced diabetic mice.
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链脲佐菌素诱导的糖尿病小鼠血浆、肝脏和肾脏中 1-磷酸鞘氨醇和载脂蛋白 M 水平的调节。

DOI:
10.1111/jdi.12232
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发表时间:
2014-11
影响因子:
3.2
通讯作者:
Yatomi Y
Yatomi Y
中科院分区:
医学3区
文献类型:
--
作者:
Nojiri T;Kurano M;Tokuhara Y;Ohkubo S;Hara M;Ikeda H;Tsukamoto K;Yatomi Y

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1-磷酸鞘氨醇(S1P)是一种多功能生物活性脂质介质,与多种疾病有关。载脂蛋白 M (ApoM) 在高密度脂蛋白上携带 S1P,并调节 S1P 代谢以增加体内 S1P 总量。 S1P 和 ApoM 都与糖尿病有关。本研究检测了链脲佐菌素诱导的糖尿病 (STZ) 小鼠血浆、肝脏和肾脏中 S1P 和 ApoM 水平的调节,以及胰岛素对 STZ 小鼠和正常小鼠血浆和肝脏中 S1P 和 ApoM 水平的影响。我们还研究了胰岛素和葡萄糖对 HepG2 细胞中 ApoM 水平的影响。 STZ 小鼠的血浆 S1P 和 ApoM 水平均高于对照小鼠。肝脏S1P和ApoM含量也升高。胰岛素治疗可降低肝脏S1P和ApoM含量,而高剂量胰岛素则降低血浆S1P和ApoM水平。在未经链脲佐菌素治疗的小鼠中,给予胰岛素降低了血浆S1P和ApoM水平以及ApoM的肝脏含量,而肝脏中的S1P水平没有改变。胰岛素治疗和低葡萄糖水平孵育降低了 HepG2 细胞中的 ApoM 水平。至于肾脏,STZ 小鼠的肾脏 S1P 和 ApoM 水平增加,胰岛素治疗部分恢复了这种增加。在 STZ 小鼠中,血浆、肝脏和肾脏中的 S1P 和 ApoM 水平升高。胰岛素治疗以某种方式逆转了 STZ 小鼠的这种调节。
Sphingosine-1-phosphate (S1P), a multifunctional bioactive lipid mediator, is involved in various diseases. Apolipoprotein M (ApoM) carries S1P on high-density lipoprotein and modulates S1P metabolism to increase the total S1P mass in the body. Both S1P and ApoM are involved in diabetes. The present study examined the modulation of S1P and ApoM levels in the plasma, liver and kidneys in streptozotocin-induced diabetes (STZ) mice, and the effects of insulin on the S1P and ApoM levels in the plasma and liver in STZ mice and normal mice. We also examined the effects of insulin and glucose on the ApoM levels in HepG2 cells. In STZ mice, both the plasma S1P and ApoM levels were higher than those in control mice. The hepatic S1P and ApoM contents were also elevated. The hepatic S1P and ApoM contents were reduced by insulin treatment, whereas high-dose insulin decreased the plasma S1P and ApoM levels. In mice without streptozotocin treatment, the administration of insulin decreased the plasma S1P and ApoM levels, and the hepatic content of ApoM, whereas the hepatic level of S1P was not altered. Treatment with insulin and incubation under a low glucose level decreased the ApoM levels in HepG2 cells. Regarding the kidney, the renal levels of S1P and ApoM were increased in STZ mice, and insulin treatment partially restored this increment. In STZ mice, the levels of S1P and ApoM in the plasma, liver, and kidneys were increased. Insulin treatment somehow reversed this modulation in STZ mice.
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发表时间: 2007-01-01
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