The effect of thyroid hormone on bile salt-independent bile flow and Na+, K+ -ATPase activity in liver plasma membranes enriched in bile canaliculi.
The effect of thyroid hormone on bile salt-independent bile flow and Na+, K+ -ATPase activity in liver plasma membranes enriched in bile canaliculi.
复制标题
甲状腺激素对不依赖胆盐的胆汁流量和胆小管中富集的肝质膜中Na，K-ATP酶活性的影响。
DOI：
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发表时间：
1976
影响因子：
15.9
通讯作者：
Boyer
中科院分区：
文献类型：
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作者：
James;L.;Boyer
在对照组、甲状腺功能亢进和甲状腺功能减退大鼠中研究了胆盐非依赖性小管流量与富含胆小管的肝细胞质膜（LPM）ATP酶活性之间的关系。与对照组（2.27 +/-0.24穆尔/min/g肝脏）相比，甲状腺功能亢进大鼠（3.19 +/-0.23穆尔/min/g肝脏）小管胆汁生成显著增加，而甲状腺功能减退动物（1.58 +/- 0.17穆尔/min/g肝脏）小管胆汁生成减少。尽管甲状腺功能亢进动物的胆盐排泄也增加（62.4 +/- 13.3 nmol/min/g肝脏vs. 41.2 +/- 8.4 nmol/min/g肝脏），但小管分泌的刺激主要与胆盐非依赖性血流分数的增强有关（甲状腺功能亢进大鼠的2.47穆尔/min/g肝脏vs.对照组的1.67穆尔/min/g肝脏）。在甲状腺功能亢进动物中，LPM Na+，K+-ATP酶活性加倍（21.5 +/- 5.8 vs. 10.7 +/- 3.1 mumol Pi/mg蛋白/h），而Mg++-ATP酶活性保持不变，5 '-核苷酸酶活性增加到较小但显著的程度。在甲状腺功能减退大鼠中，胆盐排泄与对照值相比保持不变，因此分泌减少完全继发于胆盐非依赖性分泌的抑制（1.19穆尔/min/g肝脏）。甲状腺功能减退动物的LPMs中Na+，K+-ATP酶活性降低了近50%（5.4 +/- 1.6 mumol Pi/mg蛋白/h），尽管也观察到Mg++-ATP酶和5 '-核苷酸酶比活性的类似降低。甲状腺功能减退动物的L-甲状腺素管理恢复胆汁盐独立的小管分泌和膜酶的控制值在2和4天内，分别。十二烷基硫酸钠凝胶电泳显示，任何处理组的LPM蛋白组分均无显著变化。这些研究表明，甲状腺激素对非胆盐依赖性小管分泌和LPM Na+，K+-ATP酶活性具有平行作用，支持Na+转运和Na+，K+-ATP酶可能是非胆盐依赖性小管流量的决定因素的假设。
The relationship between bile salt-independent canalicular flow and ATPase activity in liver plasma membranes (LPM) enriched in bile canaliculi, was studied in control, hyperthyroid, and hypothyroid rats. Canalicular bile production was significantly increased in hyperthyroid rats (3.19 +/- 0.23 mul/min per g liver) compared to controls (2.27 +/- 0.24 mul/min per g liver), while it diminished in hypothyroid animals (1.58 +/- 0.17 mul/min per g liver). Although bile salt excretion was also increased in hyperthyroid animals (62.4 +/- 13.3 vs. 41.2 +/- 8.4 nmol/min per g liver), the stimulation in canalicular secretion was primarily related to enhancement of the bile salt-independent fraction of flow (2.47 mul/min per g liver in hyperthyroid rats vs. 1.67 mul/min per g liver in controls). LPM Na+, K+-ATPase activity doubled in hyperthyroid animals (21.5 +/- 5.8 vs. 10.7 +/- 3.1 mumol Pi/mg protein per h) while Mg++-ATPase activity remained unchanged and 5'-nucleotidase activity increased to a small but significant extent. In hypothyroid rats, bile salt excretion remained unchanged from control values so that the reduced secretion was entirely secondary to an inhibition of bile salt-independent secretion (1.19 mul/min per g liver). Na+, K+-ATPase activity in the LPMs from hypothyroid animals decreased by nearly 50% (5.4 +/- 1.6 mumol Pi/mg protein per h), although comparable reductions in the specific activity of Mg++-ATPase and 5'-nucleotidase were also observed. Administration of L-thyroxine to hypothyroid animals restored both bile salt-independent canalicular secretion and membrane enzymes to control values within 2 and 4 days, respectively. Sodium dodecyl sulfate gel electrophoresis demonstrated no significant changes in LPM protein fractions from any of the treatment groups. These studies indicate that thyroid hormone has a parallel effect on bile salt-independent canalicular secretion and LPM Na+, K+-ATPase activity, supporting the hypothesis that Na+ transport and Na+, K+-ATPase may be determinants of bile salt-independent canalicular flow.