在正常小鼠中，葡萄糖和胰岛素可增加瘦素通过血脑屏障的转运，但在链脲佐菌素诱导的糖尿病小鼠中则不然。

Glucose and insulin increase the transport of leptin through the blood-brain barrier in normal mice but not in streptozotocin-diabetic mice.

作者信息

Kastin A J, Akerstrom V

机构信息

VA Medical Center and Tulane University School of Medicine, New Orleans, La 70112-1262, USA.

出版信息

Neuroendocrinology. 2001 Apr;73(4):237-42. doi: 10.1159/000054640.

DOI:10.1159/000054640

PMID:11340337

Abstract

Since fasting is one of the few factors found to change the rate of entry of leptin into brain, we used multiple-time regression analysis to study the effects of pretreatment with glucose or insulin on leptin transport across the blood-brain barrier (BBB). Two hours after intraperitoneal injection of glucose (3 g/kg), there was a statistically significant increase in the entry rate (K(i)) of leptin in fasted (from 4.91 +/- 0.70 x 10(-4) ml/g x min to 9.03 +/- 1.00 x 10(-4) ml/g x min) but not (p = 0.15) in nonfasted normal (from 4.90 +/- 1.21 x 10(-4) ml/g x min to 6.42 +/- 1.79 x 10(-4) ml/g x min) or fasted streptozotocin (STZ)-treated diabetic mice (from 4.043 +/- 0.959 x 10(-4) ml/g min to 5.395 +/- 1.355 x 10(-4) ml/g min). Insulin (10 U/kg) increased leptin influx in fasted (from 4.77 +/- 0.26 x 10(-4) ml/g x min to 10.6 +/- 0.15 x 10(-4) ml/g x min at 0.5 h) and nonfasted (from 4.64 +/- 0.75 x 10(-4) ml/g x min to 7.46 +/- 1.48 x 10(-4) ml/g x min at 0.5 h) normal mice, but not in STZ-diabetic mice deficient in insulin (and leptin), even though basal concentrations of glucose were similarly increased in the nonfasted normal and STZ-treated mice. Moreover, the basal rate of leptin influx was the same in overnight fasted normal mice, nonfasted normal mice and STZ-diabetic mice. The results indicate that glucose and insulin can increase leptin transport, but they probably are not the principal factors responsible for the regulatory effect of the BBB on leptin entry into the brain.

摘要

由于禁食是已发现的少数能改变瘦素进入大脑速率的因素之一，我们采用多元回归分析来研究葡萄糖或胰岛素预处理对瘦素跨血脑屏障（BBB）转运的影响。腹腔注射葡萄糖（3 g/kg）两小时后，禁食小鼠的瘦素进入速率（K(i)）有统计学显著增加（从4.91±0.70×10⁻⁴ ml/g×min增至9.03±1.00×10⁻⁴ ml/g×min），但非禁食正常小鼠（从4.90±1.21×10⁻⁴ ml/g×min增至6.42±1.79×10⁻⁴ ml/g×min，p = 0.15）或禁食链脲佐菌素（STZ）处理的糖尿病小鼠（从4.043±0.959×10⁻⁴ ml/g min增至5.395±1.355×10⁻⁴ ml/g min）则无显著增加。胰岛素（10 U/kg）增加了禁食正常小鼠（0.5小时时从4.77±0.26×10⁻⁴ ml/g×min增至10.6±0.15×10⁻⁴ ml/g×min）和非禁食正常小鼠（0.5小时时从4.64±0.75×10⁻⁴ ml/g×min增至7.46±1.48×10⁻⁴ ml/g×min）的瘦素流入，但对缺乏胰岛素（和瘦素）的STZ糖尿病小鼠无此作用，尽管非禁食正常小鼠和STZ处理小鼠的基础葡萄糖浓度同样升高。此外，过夜禁食正常小鼠、非禁食正常小鼠和STZ糖尿病小鼠的瘦素基础流入速率相同。结果表明，葡萄糖和胰岛素可增加瘦素转运，但它们可能不是血脑屏障对瘦素进入大脑起调节作用的主要因素。