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Administration of myostatin does not alter fat mass in adult mice.

机译:肌肉生长抑制素的给药不会改变成年小鼠的脂肪量。

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AIM: Myostatin, a member of the TGF-beta superfamily, is produced by skeletal muscle and acts as a negative regulator of muscle mass. It has also been suggested that low-dose administration of myostatin (2 mug/day) in rodents can reduce fat mass without altering muscle mass. In the current study, we attempted to further explore the effects of myostatin on adipocytes and its potential to reduce fat mass, since myostatin administration could potentially be a useful strategy to treat obesity and its complications in humans. METHODS: Purified myostatin protein was examined for its effects on adipogenesis and lipolysis in differentiated 3T3-L1 adipocytes as well as for effects on fat mass in wild-type, myostatin null and obese mice. RESULTS: While myostatin was capable of inhibiting adipogenesis in 3T3-L1 cells, it did not alter lipolysis in fully differentiated adipocytes. Importantly, pharmacological administration of myostatin over a range of doses (2-120 mug/day) did not affect fat mass in wild-type or genetically obese (ob/ob, db/db) mice, although muscle mass was significantly reduced at the highest myostatin dose. CONCLUSIONS: Our results suggest that myostatin does not reduce adipose stores in adult animals. Contrary to prior indications, pharmacological administration of myostatin does not appear to be an effective strategy to treat obesity in vivo.
机译:目的:肌生长抑制素是TGF-β超家族的成员,由骨骼肌产生,是肌肉质量的负调节剂。还建议在啮齿动物中低剂量施用肌肉生长抑制素(2杯/天)可以减少脂肪量而不改变肌肉量。在当前的研究中,我们试图进一步探讨肌生长抑制素对脂肪细胞的作用及其减少脂肪量的潜力,因为肌生长抑制素的给药可能是治疗肥胖症及其人类并发症的有用策略。方法:检查纯化的肌肉生长抑制素蛋白对分化的3T3-L1脂肪细胞中脂肪形成和脂解的影响以及对野生型,肌肉生长抑制素无效和肥胖小鼠脂肪含量的影响。结果:尽管肌生长抑制素能够抑制3T3-L1细胞的脂肪生成,但它并没有改变完全分化的脂肪细胞的脂解作用。重要的是,在一定剂量(2-120杯/天)的剂量范围内,肌生长抑制素的药理作用不会影响野生型或遗传性肥胖(ob / ob,db / db)小鼠的脂肪量,尽管肌肉质量在注射后显着降低。肌肉生长抑制素最高剂量。结论:我们的结果表明,肌生长抑制素不会减少成年动物的脂肪存储。与以前的适应症相反,肌生长抑制素的药理给药似乎不是体内治疗肥胖的有效策略。

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