Wiersinga W M, Chopra I J, Teco G N
Department of Medicine, UCLA Center for the Health Sciences 90024.
Metabolism. 1988 Oct;37(10):996-1002. doi: 10.1016/0026-0495(88)90159-x.
Studies were performed to evaluate a possible modulatory role of lipids on the binding of T3 to rat liver nuclear receptors in vitro. Unsaturated fatty acids were potent inhibitors of the binding of [125I] T3 to isolated rat liver nuclei. Doses (in mumol/L) causing a 50% inhibition of nuclear T3 binding were 10 for palmitoleic acid, 11 for linoleic acid, 22 for oleic acid, 24 for arachidonic acid, and 37 for linolenic acid. Other lipids had less or no inhibitory activity. Unsaturated fatty acids reduced the affinity constant (Ka) of the binding of T3 to nuclear receptors to 57.4% +/- 11.0% that of controls (mean +/- SE 1.04 +/- 0.14 v 1.97 +/- 0.23 10(9) L/M, n = 5; P less than .02) but did not affect the maximal binding capacity (MBC) (1.47 +/- 0.20 v 1.55 +/- 0.10 10(-10) M/L; NS). Evaporated ether extracts of rat liver homogenate pretreated with phospholipase A2 for five to 20 minutes (that liberates unsaturated fatty acids from phospholipids) demonstrated a progressive inhibition of nuclear T3 binding with time when compared with ether extracts of untreated rat liver homogenate (F = 16.1; P less than .01). Evaporated, fatty-acid-rich ether extracts of human sera caused a dose-dependent inhibition in the binding of [125I] T3 to nuclear T3 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
开展了多项研究以评估脂质在体外对T3与大鼠肝细胞核受体结合的潜在调节作用。不饱和脂肪酸是[125I]T3与分离的大鼠肝细胞核结合的强效抑制剂。导致核T3结合抑制50%的剂量（以μmol/L计），棕榈油酸为10，亚油酸为11，油酸为22，花生四烯酸为24，亚麻酸为37。其他脂质的抑制活性较小或无抑制活性。不饱和脂肪酸将T3与核受体结合的亲和常数（Ka）降低至对照的57.4%±11.0%（平均值±标准误1.04±0.14对1.97±0.23×10⁹L/M，n = 5；P＜0.02），但不影响最大结合容量（MBC）（1.47±0.20对1.55±0.10×10⁻¹⁰M/L；无显著性差异）。用磷脂酶A2预处理5至20分钟（从磷脂中释放不饱和脂肪酸）的大鼠肝匀浆的蒸发乙醚提取物，与未处理的大鼠肝匀浆的乙醚提取物相比，显示出随时间推移对核T3结合的进行性抑制（F = 16.1；P＜0.01）。人血清的富含脂肪酸的蒸发乙醚提取物对[125I]T3与核T3受体的结合产生剂量依赖性抑制。（摘要截短于250字）
