| 갑상샘기능저하증에 따른 생식샘기능저하증 모델 정립을 위한 제언 |
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윤상필1, 김정우2 |
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| How to design male hypothyroid hypogonadism model |
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Sang-Pil Yoon1, Jung Woo Kim2 |
Correspondence:
Jung Woo Kim, Email: kjungw1024@hanmail.net
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| Abstract |
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Hypogonadism is a clinical syndrome that results in hormone deficiency and can be classified as 1) primary caused by the gonadal failure and 2) secondary by the hypothalamus-pituitary gland dysfunction and/or cardiometabolic complications. Recently the presence of thyroid hormone receptors in different testicular cell types was demonstrated, and thus thyroid dysfunctions would be another cause of secondary hypogonadism. Thus, we investigated the effects of perinatal hypothyroidism on hypogonadism in male ICR mouse. Perinatal hypothyroidism was induced by daily administration of 0.05% 6-propyl-2-thiouracil (PTU) from gestation day 15, which were compared with negative control (PTU (-)) group. At postnatal day 28, hypothyroid pups were divided into 2 groups: PTU (+) group - continued PTU treatment and PTU (+/-) group - stopped PTU until postnatal day 49. Body weights, dehydrotesosterone (DHT), and testosterone levels were checked 2 and 3 weeks after grouping. Body weights were significantly decreased in PTU (+) and PTU (+/-) groups compared with PTU (-) group at postnatal day 28. 3 weeks later, PTU (+/-) group significantly gained weight compared with PTU (+) group. DHT and testosterone levels significantly decreased with PTU treatment, but increased 3 weeks after stopping PTU administration. Hypogonadism was induced by PTU treatment, sustained for 2 weeks after stopping PTU administration, but restored gonadal hormone levels 3 weeks after stopping PTU. These results suggest that researchers should design an experiment on hypothyroid hypogonadism based on the estimated period. |
| Key Words:
Hypogonadism, Hypothyroidism, Propylthiouracil, Mouse |
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