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Serotonin transporter deficiency increases abdominal fat in female, but not male rats.

机译:血清素转运蛋白缺乏会增加雌性大鼠的腹部脂肪,但不会增加雄性大鼠的腹部脂肪。

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摘要

Depression and abdominal obesity often co-occur, predominantly in women, and are associated with an increased risk for the development of glucose intolerance and subsequently type 2 diabetes. The underlying mechanisms are poorly understood. We found that female, but not male, depression-prone serotonin transporter knockout (SERT(-/-)) rats had a strong increase (54%) in abdominal fat, whereas no increases in plasma concentrations of glucose and insulin were observed. Surprisingly, application of a high-fat, high-sucrose (HFHS)-choice diet, which results in increased abdominal fat deposition and increased plasma glucose levels in wild-type rats, did not result in elevated plasma glucose levels in female SERT(-/-) rats. Our results show that serotonin transporter deficiency affects abdominal fat deposition in a sex-dependent way, but protects against rises in glucose levels, and thereby potentially glucose intolerance. The increased abdominal fat formation could result from serotonin-mediated developmental changes and provides heuristic value for understanding the effects of the depression-associated serotonin transporter promoter polymorphism in humans.
机译:抑郁症和腹部肥胖症通常同时发生,主要发生在女性中,并且与糖耐量异常以及随后的2型糖尿病的患病风险增加有关。根本的机制了解甚少。我们发现,雌性而不是雄性的抑郁倾向性血清素转运蛋白敲除(SERT(-/-))大鼠腹部脂肪明显增加(54%),而血浆葡萄糖和胰岛素的浓度却没有增加。令人惊讶的是,高脂,高蔗糖(HFHS)选择饮食的应用导致野生型大鼠腹部脂肪沉积增加和血浆葡萄糖水平升高,但并未导致雌性SERT血浆葡萄糖水平升高。 /-)大鼠。我们的结果表明,5-羟色胺转运蛋白缺乏症以性别相关的方式影响腹部脂肪沉积,但可防止葡萄糖水平升高,从而潜在地导致葡萄糖耐受不良。腹部脂肪形成的增加可能是由5-羟色胺介导的发育变化引起的,并为理解与抑郁相关的5-羟色胺转运蛋白启动子多态性对人的影响提供了启发性价值。

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