PMID- 17567712
OWN - NLM
STAT- MEDLINE
DCOM- 20071017
LR  - 20200930
IS  - 0363-6119 (Print)
IS  - 0363-6119 (Linking)
VI  - 293
IP  - 3
DP  - 2007 Sep
TI  - Brain-derived neurotrophic factor in the hypothalamic paraventricular nucleus 
      increases energy expenditure by elevating metabolic rate.
PG  - R992-1002
AB  - Brain-derived neurotrophic factor (BDNF) decreases food intake and body weight, 
      but few central sites of action have been identified. The hypothalamic 
      paraventricular nucleus (PVN) is important in energy metabolism regulation, and 
      expresses both BDNF and its receptor. We tested three hypotheses: 1) PVN BDNF 
      reduces feeding and increases energy expenditure (EE), 2) PVN BDNF-enhanced 
      thermogenesis results from increased spontaneous physical activity (SPA) and 
      resting metabolic rate (RMR), and 3) PVN BDNF thermogenic effects are mediated, 
      in part, by uncoupling protein 1 (UCP1) in brown adipose tissue (BAT). BDNF (0.5 
      microg) was injected into the PVN of Sprague-Dawley rats; and oxygen consumption, 
      carbon dioxide production, food intake, and SPA were measured for 24 h in an 
      indirect calorimeter. SPA was also measured in open-field activity chambers for 
      48 h after BDNF injection. Animals were killed 6 or 24 h after BDNF injection, 
      and BAT UCP1 gene expression was measured with quantitative real-time PCR. BDNF 
      significantly decreased food intake and body weight gain 24 h after injection. 
      Heat production and RMR were significantly elevated for 7 h immediately after 
      BDNF injection. BDNF had no effect on SPA, but increased UCP1 gene expression in 
      BAT at 6 h, but not 24 h after injection. In conclusion, PVN BDNF reduces body 
      weight by decreasing food intake and increasing EE consequent to increased RMR, 
      which may be due, in part, to BAT UCP1 activity. These data suggest that the PVN 
      is an important site of BDNF action to influence energy balance.
FAU - Wang, ChuanFeng
AU  - Wang C
AD  - Veterans Affairs Medical Center, Research Service (151), One Veterans Drive, 
      Minneapolis, MN 55417, USA. cwang@umn.edu
FAU - Bomberg, Eric
AU  - Bomberg E
FAU - Billington, Charles
AU  - Billington C
FAU - Levine, Allen
AU  - Levine A
FAU - Kotz, Catherine M
AU  - Kotz CM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20070613
PL  - United States
TA  - Am J Physiol Regul Integr Comp Physiol
JT  - American journal of physiology. Regulatory, integrative and comparative 
      physiology
JID - 100901230
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Ion Channels)
RN  - 0 (Mitochondrial Proteins)
RN  - 0 (Ucp1 protein, rat)
RN  - 0 (Uncoupling Protein 1)
SB  - IM
CIN - Am J Physiol Regul Integr Comp Physiol. 2007 Sep;293(3):R988-91. PMID: 17596322
MH  - Adipose Tissue, Brown/drug effects/metabolism
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/administration & dosage/*pharmacology
MH  - Calorimetry, Indirect
MH  - Eating/drug effects
MH  - Energy Metabolism/*drug effects
MH  - Ion Channels/genetics/metabolism
MH  - Kinetics
MH  - Male
MH  - Metabolism/*drug effects
MH  - Microinjections
MH  - Mitochondrial Proteins/genetics/metabolism
MH  - Motor Activity/physiology
MH  - Paraventricular Hypothalamic Nucleus/drug effects/*physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Uncoupling Protein 1
MH  - Weight Gain/drug effects
EDAT- 2007/06/15 09:00
MHDA- 2007/10/18 09:00
CRDT- 2007/06/15 09:00
PHST- 2007/06/15 09:00 [pubmed]
PHST- 2007/10/18 09:00 [medline]
PHST- 2007/06/15 09:00 [entrez]
AID - 00516.2006 [pii]
AID - 10.1152/ajpregu.00516.2006 [doi]
PST - ppublish
SO  - Am J Physiol Regul Integr Comp Physiol. 2007 Sep;293(3):R992-1002. doi: 
      10.1152/ajpregu.00516.2006. Epub 2007 Jun 13.