PMID- 25503654
OWN - NLM
STAT- MEDLINE
DCOM- 20150501
LR  - 20220321
IS  - 1349-3299 (Electronic)
IS  - 1349-2365 (Linking)
VI  - 56
IP  - 1
DP  - 2015
TI  - Calorie restriction improves cognitive decline via up-regulation of brain-derived 
      neurotrophic factor: tropomyosin-related kinase B in hippocampus 
      ofobesity-induced hypertensive rats.
PG  - 110-5
LID - 10.1536/ihj.14-168 [doi]
AB  - In metabolic syndrome (MetS), previous studies have suggested that cognitive 
      decline is worsened. Among the factors associated with cognition, decreased 
      brain-derived neurotrophic factor (BDNF) in the hippocampus causes cognitive 
      decline. We previously reported that exercise training with calorie restriction 
      yielded protection against cognitive decline via BDNF in the hippocampus of 
      hypertensive rats. The aim of the present study was to determine whether or not 
      calorie restriction results in protection against cognitive decline via BDNF and 
      its receptor tropomyosin-related kinase B (TrkB) in the hippocampus of MetS model 
      rats. We divided dietary-induced obesity-prone and hypertensive rats (OP), as 
      metabolic syndrome model rats, into three groups, fed with a high fat diet (HF), 
      treated with calorie restriction (CR) plus vehicle, and treated with CR and 
      ANA-12 (a TrkB antagonist) (CR+A). After treatment for 28 days, body weight, 
      insulin, fasting blood glucose, adiponectin, systolic blood pressure, and 
      oxidative stress in the hippocampus were significantly lower, and BDNF expression 
      in the hippocampus was significantly higher in CR and CR+A than in HF. Cognitive 
      performance determined by the Morris water maze test was significantly higher in 
      CR than in HF, whereas the benefit was attenuated in CR+A. In conclusion, calorie 
      restriction protects against cognitive decline via up-regulation of BDNF/TrkB 
      through an antioxidant effect in the hippocampus of dietary-induced obesity rats.
FAU - Kishi, Takuya
AU  - Kishi T
AD  - Department of Advanced Therapeutics for Cardiovascular Diseases, Kyushu 
      University Graduate School of Medical Sciences.
FAU - Hirooka, Yoshitaka
AU  - Hirooka Y
FAU - Nagayama, Tomomi
AU  - Nagayama T
FAU - Isegawa, Kengo
AU  - Isegawa K
FAU - Katsuki, Masato
AU  - Katsuki M
FAU - Takesue, Ko
AU  - Takesue K
FAU - Sunagawa, Kenji
AU  - Sunagawa K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141211
PL  - Japan
TA  - Int Heart J
JT  - International heart journal
JID - 101244240
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 2.7.11.28 (tropomyosin kinase)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Caloric Restriction/*methods
MH  - Cognition/physiology
MH  - *Cognition Disorders/metabolism/prevention & control
MH  - Diet, High-Fat/methods
MH  - Disease Models, Animal
MH  - Hippocampus/*metabolism
MH  - Hypertension/etiology/metabolism
MH  - Obesity/complications
MH  - Oxidative Stress/physiology
MH  - Protein Kinases/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - *Receptor, trkB/antagonists & inhibitors/metabolism
MH  - Up-Regulation
EDAT- 2014/12/17 06:00
MHDA- 2015/05/02 06:00
CRDT- 2014/12/16 06:00
PHST- 2014/12/16 06:00 [entrez]
PHST- 2014/12/17 06:00 [pubmed]
PHST- 2015/05/02 06:00 [medline]
AID - DN/JST.JSTAGE/ihj/14-168 [pii]
AID - 10.1536/ihj.14-168 [doi]
PST - ppublish
SO  - Int Heart J. 2015;56(1):110-5. doi: 10.1536/ihj.14-168. Epub 2014 Dec 11.