Bioenergetic impact of tissue-specific regulation of iodothyronine deiodinases during nutritional imbalance
Bioenergetic impact of tissue-specific regulation of iodothyronine deiodinases during nutritional imbalance
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DOI：
10.1007/s10863-011-9327-x
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发表时间：
2011-02-01
影响因子：
3
通讯作者：
Carvalho, Denise P.
中科院分区：
文献类型：
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作者：
Araujo, Renata L.;Carvalho, Denise P.
甲状腺激素对能量稳态的调节是毋庸置疑的，碘甲状腺原氨酸脱碘酶是参与这些激素在细胞水平上代谢活化或失活的酶。T3通过激素原T4的外环脱碘产生，其由1型和2型碘甲腺原氨酸脱碘酶D1和D2催化。相反，3型碘甲状腺原氨酸脱碘酶（D3）催化内环脱碘，导致T4失活为反向三碘甲状腺原氨酸（rT 3）。瘦素作为中枢和外周碘甲腺原氨酸脱碘酶的重要调节剂，从而调节T3的细胞可用性。能量负平衡时血清瘦素水平下降与肝、肾D1和BAT D2活性下调有关。此外，在高脂饮食诱导的肥胖症中，发现血清rT 3升高，而不是继发于较高的循环瘦素和促甲状腺素水平的血清T-3和T-4升高，这是可能损害氧消耗进一步增加的机制。
The regulation of energy homeostasis by thyroid hormones is unquestionable, and iodothyronine deiodinases are enzymes involved in the metabolic activation or inactivation of these hormones at the cellular level. T3 is produced through the outer ring deiodination of the prohormone T4, which is catalyzed by types 1 and 2 iodothyronine deiodinases, D1 and D2. Conversely, type 3 iodothyronine deiodinase (D3) catalyzes the inner ring deiodination, leading to the inactivation of T4 into reverse triiodothyronine (rT3). Leptin acts as an important modulator of central and peripheral iodothyronine deiodinases, thus regulating cellular availability of T3. Decreased serum leptin during negative energy balance is involved in the down regulation of liver and kidney D1 and BAT D2 activities. Moreover, in high fat diet induced obesity, instead of increased serum T-3 and T-4 secondary to higher circulating leptin and thyrotropin levels, elevated serum rT3 is found, a mechanism that might impair the further increase in oxygen consumption.