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多食和甲状腺功能减退在小鼠肥胖-高血糖综合征(ob/ob)发生发展中的作用。

The role of hyperphagia and hypothyroidism in the development of the obese-hyperglycemic syndrome in mice (ob/ob).

作者信息

van der Kroon P H, Wittgen-Struik G, Vermeulen L

出版信息

Int J Obes. 1981;5(4):353-8.

PMID:6946982
Abstract

Obese-hyperglycemic mice show hyperphagia and hypothyroidism. The reduced body temperature can be normalized by injection of thyroxin. Limiting food intake to normal non-obese levels reduces blood sugar level, insulin content of the blood and body weight. However, reduction of all these parameters together until normal level occurs only when combining thyroxin injection with restricted diet. Weight of epididymal fat pad, nuclear volume of Leydig cells and volumes of islets of Langerhans normalize too during the combined treatment. It is argued that in adult obese mice hyperphagia and hypothyroidism are two separate factors which cannot be completely compensated for one by another. At least some symptoms in the obese-hyperglycemic syndrome could be attributed to hypothalamic disturbances caused by a reduced thyroidal activity at a very early age after birth.

摘要

肥胖高血糖小鼠表现出食欲亢进和甲状腺功能减退。注射甲状腺素可使降低的体温恢复正常。将食物摄入量限制在正常非肥胖水平可降低血糖水平、血液中的胰岛素含量和体重。然而,只有在将甲状腺素注射与限制饮食相结合时,所有这些参数才会一起降至正常水平。在联合治疗期间,附睾脂肪垫重量、睾丸间质细胞核体积和胰岛体积也恢复正常。有人认为,在成年肥胖小鼠中,食欲亢进和甲状腺功能减退是两个独立的因素,不能相互完全代偿。肥胖高血糖综合征的至少一些症状可能归因于出生后很早年龄甲状腺活动降低引起的下丘脑紊乱。

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