PMID- 19748969
OWN - NLM
STAT- MEDLINE
DCOM- 20100118
LR  - 20220331
IS  - 1469-445X (Electronic)
IS  - 0958-0670 (Linking)
VI  - 94
IP  - 12
DP  - 2009 Dec
TI  - Role of exercise-induced brain-derived neurotrophic factor production in the 
      regulation of energy homeostasis in mammals.
PG  - 1153-60
LID - 10.1113/expphysiol.2009.048561 [doi]
AB  - 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.
FAU - Pedersen, Bente K
AU  - Pedersen BK
AD  - Centre of Inflammation and Metabolism, Rigshospitalet-Section 7641, Blegdamsvej 
      9, DK-2100, Copenhagen, Denmark. bkp@rh.dk
FAU - Pedersen, Maria
AU  - Pedersen M
FAU - Krabbe, Karen S
AU  - Krabbe KS
FAU - Bruunsgaard, Helle
AU  - Bruunsgaard H
FAU - Matthews, Vance B
AU  - Matthews VB
FAU - Febbraio, Mark A
AU  - Febbraio MA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20090911
PL  - England
TA  - Exp Physiol
JT  - Experimental physiology
JID - 9002940
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
SB  - IM
MH  - AMP-Activated Protein Kinases/metabolism
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/biosynthesis/*physiology
MH  - Diabetes Mellitus, Type 2/metabolism
MH  - Energy Metabolism/drug effects/*physiology
MH  - Exercise/physiology
MH  - Homeostasis
MH  - Humans
MH  - Lipid Metabolism
MH  - Muscle Contraction/physiology
MH  - Muscle, Skeletal/metabolism
MH  - Neurodegenerative Diseases/physiopathology
MH  - Physical Conditioning, Animal/physiology
RF  - 51
EDAT- 2009/09/15 06:00
MHDA- 2010/01/19 06:00
CRDT- 2009/09/15 06:00
PHST- 2009/09/15 06:00 [entrez]
PHST- 2009/09/15 06:00 [pubmed]
PHST- 2010/01/19 06:00 [medline]
AID - expphysiol.2009.048561 [pii]
AID - 10.1113/expphysiol.2009.048561 [doi]
PST - ppublish
SO  - Exp Physiol. 2009 Dec;94(12):1153-60. doi: 10.1113/expphysiol.2009.048561. Epub 
      2009 Sep 11.