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肥胖(ob/ob)小鼠的一种酶缺陷:甲状腺诱导的钠钾依赖型三磷酸腺苷酶缺失。

An enzymatic defect in the obese (ob/ob) mouse: loss of thyroid-induced sodium- and potassium-dependent adenosinetriphosphatase.

作者信息

York D A, Bray G A, Yukimura Y

出版信息

Proc Natl Acad Sci U S A. 1978 Jan;75(1):477-81. doi: 10.1073/pnas.75.1.477.

DOI:10.1073/pnas.75.1.477
PMID:146880
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC411273/
Abstract

Genetically obese (ob/ob) mice, mice that became obese after treatment with gold thioglucose, and lean animals were studied in the euthyroid state, after induction of hypothyroidism, and after treatment with triiodothyronine. The activity of glycerol 3-phosphate dehydrogenase (sn-glycerol-3-phosphate:(acceptor) oxidoreductase; EC 1.1.99.5] was reduced in the livers from hypothyroid animals and was increased by treatment with triiodothyronine in all groups. The activity of the ouabain-suppressible sodium- and potassium-dependent ATPase (ATP phosphohydrolase; EC 3.6.1.3) was increased by triiodothyronine and reduced by hypothyroidism in the lean and gold thioglucose-treated obese animals. In the obese (ob/ob) mice, on the other hand, treatment with triiodothyronine did not increase the activity of this enzyme, which remained at the level found in hypothyroid animals. This enzymatic activity was reduced in both liver and kidney. Adenylate cyclase [ATP pyrophosphate-lyase (cyclizing); EC 4.6.1.1] activity in liver membranes, however, was similar in all three groups of mice. This enzyme complex was activated by glucagon and was unaffected by treatment with thyroid hormones. The lack of a thyroid-dependent ouabain-suppressible (Na(+) + K(+))-ATPase in the tissues of the obese (ob/ob) mouse could explain most, if not all, of the abnormalities that have been described in this animal.

摘要

对遗传性肥胖(ob/ob)小鼠、经硫代葡萄糖金处理后变得肥胖的小鼠以及瘦小鼠在甲状腺功能正常状态、甲状腺功能减退诱导后以及用三碘甲状腺原氨酸治疗后进行了研究。甲状腺功能减退动物肝脏中甘油3-磷酸脱氢酶(sn-甘油-3-磷酸:(受体)氧化还原酶;EC 1.1.99.5)的活性降低,且在所有组中用三碘甲状腺原氨酸治疗后该活性均升高。在瘦小鼠和经硫代葡萄糖金处理的肥胖小鼠中,哇巴因可抑制的钠钾依赖性ATP酶(ATP磷酸水解酶;EC 3.6.1.3)的活性因三碘甲状腺原氨酸而升高,因甲状腺功能减退而降低。另一方面,在肥胖(ob/ob)小鼠中,用三碘甲状腺原氨酸治疗并未增加该酶的活性,其仍保持在甲状腺功能减退动物中所发现的水平。这种酶活性在肝脏和肾脏中均降低。然而,三组小鼠肝细胞膜中的腺苷酸环化酶[ATP焦磷酸裂解酶(环化);EC 4.6.1.1]活性相似。该酶复合物被胰高血糖素激活,且不受甲状腺激素治疗的影响。肥胖(ob/ob)小鼠组织中缺乏甲状腺依赖性的哇巴因可抑制的(Na(+) + K(+))-ATP酶,这可以解释该动物中所描述的大部分(如果不是全部)异常情况。

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An enzymatic defect in the obese (ob/ob) mouse: loss of thyroid-induced sodium- and potassium-dependent adenosinetriphosphatase.肥胖(ob/ob)小鼠的一种酶缺陷:甲状腺诱导的钠钾依赖型三磷酸腺苷酶缺失。
Proc Natl Acad Sci U S A. 1978 Jan;75(1):477-81. doi: 10.1073/pnas.75.1.477.
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Protein measurement with the Folin phenol reagent.使用福林酚试剂进行蛋白质测定。
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