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脑源性神经营养因子类似物通过增强骨骼肌中线粒体生物发生来减轻肥胖小鼠的体重增加。

BDNF mimetic alleviates body weight gain in obese mice by enhancing mitochondrial biogenesis in skeletal muscle.

机构信息

Department of Physiology, the University of Oklahoma Health Sciences Center, Oklahoma City, USA.

School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, China.

出版信息

Metabolism. 2018 Oct;87:113-122. doi: 10.1016/j.metabol.2018.06.007. Epub 2018 Jun 20.

Abstract

BACKGROUND

7,8-Dihydroxyflavone (7,8-DHF) is a small molecular weight compound that mimics the functions of brain-derived neurotrophic factor (BDNF). The current study aims to elucidate the molecular mechanism of 7,8-DHF-induced body weight regulation.

METHODS

Obese female C57/BL6 (20-week-old) mice that have been fed with high-fat diet for 13 weeks were treated with 7,8-DHF for 9 weeks. Various biochemical and molecular analyses were performed to examine the signal transduction pathway, metabolite content, and mitochondrial mass in the animals. Moreover, systemic energy metabolism and insulin sensitivity were determined by indirect calorimetry and insulin/glucose-tolerance tests. We have also determined the metabolic actions of 7,8-DHF on cultured myotubes.

RESULTS

7,8-DHF treatment increased cellular respiration by promoting mitochondrial biogenesis in cultured skeletal muscle cells. In diet-induced obese mice, subsequent 7,8-DHF consumption triggered the AMPK/CREB/PGC-1α pathways to increase the muscular mitochondrial content. Systemic energy metabolism was thus elevated, which reduced the body weight gain in obese animals. Consequently, hyperlipidemia, hyperglycemia hyperinsulinemia, and ectopic lipid accumulation in skeletal muscle and liver of the obese animals were alleviated after 7,8-DHF treatment. Moreover, insulin sensitivity of the obese muscle was improved after 7,8-DHF consumption.

CONCLUSION

7,8-DHF treatment increases muscular mitochondrial respiration and systemic energy expenditure, which alleviates the body weight gain and partially reverse the metabolic abnormalities induced by obesity.

摘要

背景

7,8-二羟基黄酮(7,8-DHF)是一种模拟脑源性神经营养因子(BDNF)功能的小分子化合物。本研究旨在阐明 7,8-DHF 诱导体重调节的分子机制。

方法

13 周高脂饮食喂养的肥胖雌性 C57/BL6(20 周龄)小鼠用 7,8-DHF 治疗 9 周。进行各种生化和分子分析,以检查动物中的信号转导途径、代谢物含量和线粒体质量。此外,通过间接测热法和胰岛素/葡萄糖耐量试验测定全身能量代谢和胰岛素敏感性。我们还确定了 7,8-DHF 在培养的肌管上的代谢作用。

结果

7,8-DHF 处理通过促进培养的骨骼肌细胞中线粒体生物发生来增加细胞呼吸。在饮食诱导的肥胖小鼠中,随后的 7,8-DHF 消耗触发 AMPK/CREB/PGC-1α 途径增加肌肉中线粒体的含量。因此,全身能量代谢增加,从而减少肥胖动物的体重增加。因此,7,8-DHF 治疗后肥胖动物的高脂血症、高血糖、高胰岛素血症和骨骼肌和肝脏中的异位脂质积累得到缓解。此外,7,8-DHF 消耗后肥胖肌肉的胰岛素敏感性得到改善。

结论

7,8-DHF 治疗增加肌肉线粒体呼吸和全身能量消耗,减轻体重增加,并部分逆转肥胖引起的代谢异常。

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