Katoh H, Kawashima Y, Takegishi M, Watanuki H, Hirose A, Kozuka H
Res Commun Chem Pathol Pharmacol. 1985 Aug;49(2):229-41.
Inductions of FABP in hepatic cytosol by administration of tiadenol and clofibric acid were studied in rats, mice and guinea-pigs. In rats and mice, [1-14C]oleic acid-binding capacity of hepatic cytosol was increased, in association with induction of peroxisomal beta-oxidation, by the administration of either the two peroxisome proliferators. The increase in [1-14C]oleic acid binding capacity was responsible for the increase in the content of FABP in livers. The peroxisome proliferators caused an induction of acyl-CoA hydrolase of lower-molecular-weight form alone in hepatic cytosol of mice, although inductions of two long-chain acyl-CoA hydrolases (higher- and lower-molecular-weight form) were brought about in hepatic cytosol of rats. Guinea-pigs lacked the peroxisome proliferator-caused inductions of FABP, peroxisomal beta-oxidation and acyl-CoA hydrolase. There was no essential difference in the inductions of FABP, acyl-CoA hydrolases and peroxisomal beta-oxidation between tiadenol and clofibric acid, despite a marked difference in their chemical structures. These results suggest that the induction of FABP is correlated with the inductions of both peroxisomal beta-oxidation and cytosolic long-chain acyl-CoA hydrolase of lower-molecular-weight form.
在大鼠、小鼠和豚鼠中研究了给予替阿地诺和氯贝酸后肝胞质溶胶中脂肪酸结合蛋白（FABP）的诱导情况。在大鼠和小鼠中，给予这两种过氧化物酶体增殖剂后，肝胞质溶胶的[1-¹⁴C]油酸结合能力增加，这与过氧化物酶体β氧化的诱导相关。[1-¹⁴C]油酸结合能力的增加导致肝脏中FABP含量增加。过氧化物酶体增殖剂仅在小鼠肝胞质溶胶中诱导出低分子量形式的酰基辅酶A水解酶，而在大鼠肝胞质溶胶中则诱导出两种长链酰基辅酶A水解酶（高分子量和低分子量形式）。豚鼠缺乏过氧化物酶体增殖剂引起的FABP、过氧化物酶体β氧化和酰基辅酶A水解酶的诱导。尽管替阿地诺和氯贝酸的化学结构有显著差异，但它们在FABP、酰基辅酶A水解酶和过氧化物酶体β氧化的诱导方面没有本质区别。这些结果表明，FABP的诱导与过氧化物酶体β氧化和低分子量形式的胞质长链酰基辅酶A水解酶的诱导相关。
