Tissue-specific regulation of 11β hydroxysteroid dehydrogenase type-1 mRNA expressions in Cushing's syndrome mouse model

被引：3

作者：

Nishiyama, Mitsuru ^{[1
,2
]}

Iwasaki, Yasumasa ^{[1
,5
]}

Nakayama, Shuichi ^{[1
,6
]}

Okazaki, Mizuho ^{[3
]}

Taguchi, Takafumi ^{[1
]}

Tsuda, Masayuki ^{[4
]}

Makino, Shinya ^{[1
,7
]}

Fujimoto, Shimpei ^{[1
]}

Terada, Yoshio ^{[1
]}

机构：

[1] Kochi Univ, Kochi Med Sch, Dept Endocrinol Metab & Nephrol, 1-185 Kohasu,Oko cho, Nankoku, Kochi 7838505, Japan

[2] Kochi Univ, Hlth Care Ctr, 1-5-2 Akebono cho, Kochi, Kochi 7808520, Japan

[3] Kochi Univ, Kochi Med Sch, Dept Clin Lab, 1-185 Kohasu,Oko cho, Nankoku, Kochi 7838505, Japan

[4] Kochi Univ, Kochi Med Sch, Dept Lab Anim Sci, 1-185 Kohasu,Oko cho, Nankoku, Kochi 7838505, Japan

[5] Suzuka Univ Med Sci, Fac Hlth Sci, Dept Clin Nutr, 1-1001 Kishioka cho, Suzuka, Mie 5100293, Japan

[6] Chikamori Hosp, Dept Internal Med, 16-1-1 Okawasuji, Kochi, Kochi 7808522, Japan

[7] Osaka Gyomeikan Hosp, Dept Internal Med, 5-4-8 Nishikujo,Konohana ku, Osaka, Osaka 5540012, Japan

来源：

STEROIDS | 2022年 / 183卷

关键词：

Glucocorticoid; Hippocampus; Liver; Fat; 11 beta-Hydroxysteroid dehydrogenase type-1; Cushing's syndrome; METABOLIC SYNDROME; VISCERAL OBESITY; CORTICOSTERONE; GLUCOCORTICOIDS; CORTISOL; RECEPTOR; DIFFERENTIATION; IMPLANTATION; INSULIN; MICE;

D O I：

10.1016/j.steroids.2022.109021

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The 11 beta hydroxysteroid dehydrogenase type-1 (11 beta HSD-1) is a predominant 11 beta-reductase regenerating bioactive glucocorticoids (cortisol, corticosterone) from inactive 11-keto forms (cortisone, dehydrocorticosterone), expressed mainly in the brain, liver and adipose tissue. Although the expression levels of 11 beta HSD-1 mRNA are known to be influenced by glucocorticoids, its tissue-specific regulation is not completely elucidated. In this study, we examined the effect of persistent glucocorticoid excess on the expression of 11 beta HSD-1 mRNA in the hippocampus, liver, and abdominal adipose tissue in vivo using quantitative real-time PCR. We found that, in C57BL/6J mice treated with corticosterone (CORT) pellet for 2 weeks, 11 beta HSD-1 mRNA decreased in the hippocampus (HIPP) and liver, whereas it increased in the abdominal fat (FAT), compared with placebo treatment [HIPP: placebo 1.00 +/- 0.14, CORT 0.63 +/- 0.04; liver: placebo 1.00 +/- 0.08, CORT 0.73 +/- 0.06; FAT: placebo 1.00 +/- 0.16, CORT 2.26 +/- 0.39]. Moreover, in CRH transgenic mice, an animal model of Cushing's syndrome with high plasma CORT level, 11 beta HSD-1 mRNA was also decreased in the hippocampus and liver, and increased in the abdominal adipose tissue compared to that in wild-type mice. These changes were reversed after adrenalectomy in CRH-Tg mice. Altogether, these results reveal the differential regulation of 11 beta HSD-1 mRNA by glucocorticoid among the tissues examined.

引用

页数：7

共 43 条

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