Telmisartan prevents obesity and increases the expression of uncoupling protein 1 in diet-induced obese mice

Telmisartan prevents obesity and increases the expression of uncoupling protein 1 in diet-induced obese mice
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DOI:
10.1161/01.hyp.0000225402.69580.1d
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发表时间:
2006-07-01
期刊:
影响因子:
8.3
通讯作者:
Yoshimatsu, Hironobu
Yoshimatsu, Hironobu
中科院分区:
医学1区
文献类型:
--
作者:
Araki, Kana;Masaki, Takayuki;Yoshimatsu, Hironobu

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本研究旨在阐明替米沙坦(一种血管紧张素II受体阻滞剂)对饮食诱导肥胖小鼠肥胖和相关代谢紊乱的影响。与使用未处理水的对照组相比,以5 mg/kg/天的剂量将替米沙坦溶于饮用水,持续14天,可减弱饮食诱导的肥胖小鼠的体重增加,而不影响摄食量。替米沙坦治疗降低了内脏脂肪组织的重量以及肝脏和骨骼肌中的甘油三酯含量。此外,饮食诱导肥胖小鼠的高血糖症、高胰岛素血症和高胆固醇血症均在替米沙坦治疗后得到改善。此外,替米沙坦治疗增加了内脏白色脂肪组织中的脂联素mRNA,并伴随血清脂联素水平的变化。与此相反,治疗降低了血清中β-内酰胺酶的水平。最后,替米沙坦治疗增加了棕色脂肪组织中解偶联蛋白1的mRNA表达,并伴有耗氧量增加。总之,在饮食诱导的肥胖小鼠中,替米沙坦治疗可能通过改变脂联素、β-内酰胺酶和解偶联蛋白1的水平来预防肥胖和相关代谢紊乱的发生。我们的研究结果表明,替米沙坦可作为代谢综合征,包括内脏肥胖的治疗工具。
The aim of the present study was to clarify the effect of telmisartan, an angiotensin II receptor blocker, on the development of obesity and related metabolic disorders in diet-induced obese mice. Treatment with telmisartan dissolved in drinking water at a dosage of 5 mg/kg per day for 14 days attenuated the diet-induced weight gain without affecting food intake in diet-induced obese mice compared with controls using nontreated water. Telmisartan treatment decreased the weight of visceral adipose tissue and the triglyceride content in the liver and skeletal muscle. In addition, hyperglycemia, hyperinsulinemia, and hypertriglyceridemia in diet-induced obese mice all improved with telmisartan treatment. Furthermore, telmisartan treatment increased adiponectin mRNA in visceral white adipose tissue and was associated with a concomitant change in the serum adiponectin level. In contrast, the treatment reduced the serum level of resistin. Finally, telmisartan treatment increased the mRNA expression of uncoupling protein 1 in brown adipose tissue and was accompanied by an increase in oxygen consumption. In conclusion, telmisartan treatment might prevent the development of obesity and related metabolic disorders by altering the levels of adiponectin, resistin, and uncoupling protein 1 in diet-induced obese mice. Our results indicate that telmisartan can be used as a therapeutic tool for metabolic syndrome, including visceral obesity.