Phosphatidic acid and phosphatidylinositol labelling in adipose tissue. The role of endogenously formed adenosine.
Phosphatidic acid and phosphatidylinositol labelling in adipose tissue. The role of endogenously formed adenosine.
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脂肪组织中的磷脂酸和磷脂酰肌醇标记。
DOI：
10.1042/bj2120499
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
McMahon,KK
中科院分区：
文献类型：
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作者：
Schimmel,RJ;Honeyman,TW;McMahon,KK
3-异丁基-1-甲基黄嘌呤部分抑制[~（32）P]Pi掺入仓鼠附睾脂肪细胞的磷脂酸和磷脂酰肌醇。异丙基-N6-苯腺苷可拮抗3-异丁基-1-甲基黄嘌呤的这种作用，而2′，5 ′-二脱氧腺苷、前列腺素E1或可乐定则不拮抗。当3-异丁基-1-甲基黄嘌呤不存在时，N6-Phenylisopropyladenosine不影响[32 P]Pi掺入磷脂酸或磷脂酰肌醇。3-异丁基-1-甲基黄嘌呤对[32 P]Pi掺入磷脂的抑制作用仅被N6-苯基异丙基腺苷阻断，而前列腺素E1、可乐定和2′，5 ′-双脱氧腺苷以及N6-苯基异丙基腺苷均能阻断加速脂解。磷脂标记也减少腺苷脱氨酶的存在下，但不存在异丙肾上腺素（异丙肾上腺素）。N6-phenylisopropyladenosine对[32 P]Pi掺入暴露于3-异丁基-1-甲基黄嘌呤的细胞中的磷脂的刺激作用是显而易见的，只要3分钟后加入的腺苷类似物和最大10分钟后，其添加。正如其他人所观察到的，α 1-选择性激动剂甲氧胺增加了[32 P]Pi掺入磷脂中。甲氧胺的刺激作用发生的时间过程类似于N6-苯基异丙基腺苷，并在3-异丁基-1-甲基黄嘌呤的存在或不存在下以几乎相等的幅度存在。3-异丁基-1-甲基黄嘌呤和腺苷脱氨酶对磷脂标记的抑制作用归因于阻断作用，或酶促去除脂肪细胞在孵育期间形成和释放的腺苷。支持这一观点的是N6-phenylisopropyladenosine选择性逆转3-异丁基-1-甲基黄嘌呤和腺苷脱氨酶的作用。这些发现表明内源性腺苷在调节脂肪细胞磷脂周转中的重要作用。
Incorporation of [32P]Pi into phosphatidic acid and phosphatidylinositol of hamster epididymal adipocytes was partially inhibited by 3-isobutyl-1-methylxanthine. This effect of 3-isobutyl-1-methylxanthine was antagonized by isopropyl-N6-phenyladenosine but not by 2′,5′-dideoxyadenosine, prostaglandin E1 or clonidine. N6-Phenylisopropyladenosine did not affect incorporation of [32P]Pi into phosphatidic acid or phosphatidylinositol when 3-isobutyl-1-methylxanthine was not present. In contrast with 3-isobutyl-1-methylxanthine inhibition of [32P]Pi incorporation into phospholipids, which was blocked only by N6-phenylisopropyladenosine, accelerated lipolysis was blocked by prostaglandin E1, clonidine and 2′,5′-dideoxyadenosine as well as by N6-phenylisopropyladenosine. Phospholipid labelling was also decreased in the presence of adenosine deaminase, but not in the presence of isoprenaline (isoproterenol). The stimulatory effect of N6-phenylisopropyladenosine on [32P]Pi incorporation into phospholipids in cells exposed to 3-isobutyl-1-methylxanthine was evident as soon as 3 min after addition of the adenosine analogue and maximum 10 min after its addition. As observed by others, [32P]Pi incorporation into phospholipids was increased by the alpha 1-selective agonist methoxamine. The stimulatory effect of methoxamine occurred with a time course similar to that of N6-phenylisopropyladenosine and was present at nearly equal magnitude in the absence or presence of 3-isobutyl-1-methylxanthine. The inhibitory effects of 3-isobutyl-1-methylxanthine and adenosine deaminase on phospholipid labelling are attributed to blockade of the action, or to the enzymic removal, of adenosine formed in and released from the fat-cells during their incubation. Supporting this view is the selective reversal of the actions of 3-isobutyl-1-methylxanthine and of adenosine deaminase by N6-phenylisopropyladenosine. These findings suggest an important role for endogenous adenosine in regulation of phospholipid turnover in adipocytes.