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牛磺酸(2-氨基乙磺酸)缺乏会形成一个促进肥胖的恶性循环。

Taurine (2-aminoethanesulfonic acid) deficiency creates a vicious circle promoting obesity.

作者信息

Tsuboyama-Kasaoka Nobuyo, Shozawa Chikako, Sano Kayo, Kamei Yasutomi, Kasaoka Seiichi, Hosokawa Yu, Ezaki Osamu

机构信息

Division of Clinical Nutrition, National Institute of Health and Nutrition, 1-23-1 Toyama, Tokyo 162-8636, Japan.

出版信息

Endocrinology. 2006 Jul;147(7):3276-84. doi: 10.1210/en.2005-1007. Epub 2006 Apr 20.

DOI:10.1210/en.2005-1007
PMID:16627576
Abstract

The relation between blood taurine (2-aminoethanesulfonic acid) concentrations and obesity was investigated. Taurine is supplied to the body by dietary ingestion as well as by de novo synthesis; it is anabolized by cysteine dioxygenase (CDO), which is abundantly expressed in liver and white adipose tissue. Overexpression of CDO in 3T3-L1 preadipocytes caused a decrease in the level of cysteine (precursor of taurine) and an increase in the level of taurine in the culture medium, suggesting that CDO is involved in biosynthesis and secretion of taurine in white adipose tissue. In high-fat diet-induced and/or genetically obese mice, a decrease in the blood taurine concentration was observed along with a decrease in CDO expression in adipose tissue but not in liver. Dietary taurine supplementation prevented high-fat diet-induced obesity with increased resting energy expenditure. Thus, taurine deficiency observed in association with obesity may create a vicious circle promoting obesity. Dietary taurine supplementation interrupts this vicious circle and may prevent obesity.

摘要

研究了血液中牛磺酸(2-氨基乙磺酸)浓度与肥胖之间的关系。牛磺酸可通过饮食摄入以及从头合成提供给身体;它由半胱氨酸双加氧酶(CDO)合成代谢,该酶在肝脏和白色脂肪组织中大量表达。在3T3-L1前脂肪细胞中过表达CDO导致培养基中半胱氨酸(牛磺酸前体)水平降低,牛磺酸水平升高,这表明CDO参与白色脂肪组织中牛磺酸的生物合成和分泌。在高脂饮食诱导和/或基因肥胖小鼠中,观察到血液中牛磺酸浓度降低,同时脂肪组织而非肝脏中的CDO表达降低。补充膳食牛磺酸可预防高脂饮食诱导的肥胖,并增加静息能量消耗。因此,与肥胖相关的牛磺酸缺乏可能会形成一个促进肥胖的恶性循环。补充膳食牛磺酸可中断这个恶性循环并可能预防肥胖。

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