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运动诱导的脑源性神经营养因子产生在哺乳动物能量平衡调节中的作用。

Role of exercise-induced brain-derived neurotrophic factor production in the regulation of energy homeostasis in mammals.

机构信息

Centre of Inflammation and Metabolism, Rigshospitalet-Section 7641, Blegdamsvej 9, DK-2100, Copenhagen, Denmark.

出版信息

Exp Physiol. 2009 Dec;94(12):1153-60. doi: 10.1113/expphysiol.2009.048561. Epub 2009 Sep 11.

DOI:10.1113/expphysiol.2009.048561
PMID:19748969
Abstract

Brain-derived neurotrophic factor (BDNF) has been shown to regulate neuronal development and plasticity and plays a role in learning and memory. Moreover, it is well established that BDNF plays a role in the hypothalamic pathway that controls body weight and energy homeostasis. Recent evidence identifies BDNF as a player not only in central metabolism, but also in regulating energy metabolism in peripheral organs. Low levels of BDNF are found in patients with neurodegenerative diseases, including Alzheimer's disease and major depression. In addition, BDNF levels are low in obesity and independently so in patients with type 2 diabetes. Brain-derived neurotrophic factor is expressed in non-neurogenic tissues, including skeletal muscle, and exercise increases BDNF levels not only in the brain and in plasma, but in skeletal muscle as well. Brain-derived neurotrophic factor mRNA and protein expression was increased in muscle cells that were electrically stimulated, and BDNF increased phosphorylation of AMP-activated protein kinase (AMPK) and acetyl coenzyme A carboxylase-beta (ACCbeta) and enhanced fatty oxidation both in vitro and ex vivo. These data identify BDNF as a contraction-inducible protein in skeletal muscle that is capable of enhancing lipid oxidation in skeletal muscle via activation of AMPK. Thus, BDNF appears to play a role both in neurobiology and in central as well as peripheral metabolism. The finding of low BDNF levels both in neurodegenerative diseases and in type 2 diabetes may explain the clustering of these diseases. Brain-derived neurotrophic factor is likely to mediate some of the beneficial effects of exercise with regard to protection against dementia and type 2 diabetes.

摘要

脑源性神经营养因子(BDNF)已被证明可调节神经元发育和可塑性,并在学习和记忆中发挥作用。此外,BDNF 在控制体重和能量平衡的下丘脑途径中发挥作用已得到充分证实。最近的证据表明,BDNF 不仅是中央代谢的参与者,而且还调节外周器官的能量代谢。在包括阿尔茨海默病和重度抑郁症在内的神经退行性疾病患者中发现 BDNF 水平降低。此外,肥胖症患者的 BDNF 水平较低,2 型糖尿病患者也是如此。BDNF 表达于非神经生成组织,包括骨骼肌,运动不仅可增加大脑和血浆中的 BDNF 水平,还可增加骨骼肌中的 BDNF 水平。电刺激肌细胞可增加 BDNF mRNA 和蛋白表达,BDNF 可增加 AMP 激活蛋白激酶(AMPK)和乙酰辅酶 A 羧化酶-β(ACCβ)的磷酸化,并增强体外和体内的脂肪酸氧化。这些数据表明,BDNF 是一种可诱导收缩的骨骼肌蛋白,可通过激活 AMPK 增强骨骼肌中的脂质氧化。因此,BDNF 似乎在神经生物学以及中枢和外周代谢中都发挥作用。在神经退行性疾病和 2 型糖尿病中发现的 BDNF 水平降低可能解释了这些疾病的聚集。BDNF 可能介导了运动对预防痴呆症和 2 型糖尿病的一些有益作用。

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