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糖尿病会增强肝细胞膜囊泡中丙氨酸转运的活性。

Diabetes enhances activity of alanine transport in liver plasma membrane vesicles.

作者信息

Rosenthal N R, Jacob R, Barrett E

出版信息

Am J Physiol. 1985 May;248(5 Pt 1):E581-7. doi: 10.1152/ajpendo.1985.248.5.E581.

Abstract

In the present study plasma membrane vesicles were prepared from livers of control and alloxan-induced diabetic rats and the substrate specificity and kinetic characteristics of alanine transport determined in both groups. Sodium-dependent alanine uptake at physiological alanine concentrations (100 microM) was enhanced threefold in diabetic as compared with control animals (0.31 +/- 0.04 vs. 0.11 +/- 0.01 nmol X mg protein-1 X 10 s-1). This accelerated influx corresponded to a three- to fourfold increase in the Vmax of alanine transport in diabetic versus control group (7.1 +/- 2.1 vs. 1.6 +/- 0.2 nmol X mg protein-1 X 10 s-1, P less than 0.05), whereas the Km of alanine uptake was unchanged (2.8 +/- 1.2 vs. 1.4 +/- 0.1 mM). Other neutral amino acids (20 mM) inhibited alanine transport to a similar degree in both groups. The sodium-dependent influx of glutamine (100 microM) was similar in diabetic and control groups (0.17 +/- 0.03 and 0.14 +/- 0.02 nmol X mg protein-1 X 10 s-1, respectively). The initial velocity of 22Na uptake (80 mM) into vesicles and half-maximal stimulation of alanine transport was achieved at essentially identical sodium concentrations (approximately 40 mM) in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在本研究中,从对照大鼠和四氧嘧啶诱导的糖尿病大鼠的肝脏中制备了质膜囊泡,并测定了两组中丙氨酸转运的底物特异性和动力学特征。与对照动物相比,糖尿病动物在生理丙氨酸浓度(100微摩尔)下钠依赖性丙氨酸摄取增加了两倍(0.31±0.04对0.11±0.01纳摩尔×毫克蛋白-1×10秒-1)。这种加速流入对应于糖尿病组与对照组丙氨酸转运Vmax增加了三到四倍(7.1±2.1对1.6±0.2纳摩尔×毫克蛋白-1×10秒-1,P<0.05),而丙氨酸摄取的Km不变(2.8±1.2对1.4±0.1毫摩尔)。其他中性氨基酸(20毫摩尔)在两组中对丙氨酸转运的抑制程度相似。糖尿病组和对照组中谷氨酰胺(100微摩尔)的钠依赖性流入相似(分别为0.17±0.03和0.14±0.02纳摩尔×毫克蛋白-1×10秒-1)。两组中,囊泡对22Na的摄取(80毫摩尔)的初始速度和丙氨酸转运的半最大刺激在基本相同的钠浓度(约40毫摩尔)下实现。(摘要截断于250字)

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