PMID- 25771935
OWN - NLM
STAT- MEDLINE
DCOM- 20160226
LR  - 20220321
IS  - 1365-2826 (Electronic)
IS  - 0953-8194 (Linking)
VI  - 27
IP  - 5
DP  - 2015 May
TI  - Brain-derived neurotrophic factor and substrate utilization following acute 
      aerobic exercise in obese individuals.
PG  - 370-6
LID - 10.1111/jne.12275 [doi]
AB  - Brain-derived neurotrophic factor (BDNF) serves as a vital regulator of neuronal 
      proliferation and survival, and has been shown to regulate energy homeostasis, 
      glucose metabolism and body weight maintenance. Elevated concentrations of plasma 
      BDNF have been associated with obesity and type 2 diabetes mellitus. Acute 
      aerobic exercise transiently increases circulating BDNF, potentially correcting 
      obesity-related metabolic impairment. The present study aimed to compare acute 
      aerobic exercise elicited BDNF responses in obese and normal-weight subjects. 
      Furthermore, we aimed to investigate whether acute exercise-induced plasma BDNF 
      elevations would be associated with improved indices of insulin resistance, as 
      well as substrate utilization [carbohydrate oxidation (CHOoxi) and fat oxidation 
      (FAToxi)]. Twenty-two healthy, untrained subjects [11 obese (four men and seven 
      women; age = 22.91 +/- 4.44 years; body mass index = 35.72 +/- 4.17 kg/m(2)) and 11 
      normal-weight (five men and six women; age = 23.27 +/- 2.24 years; body mass index 
      = 21.89 +/- 1.63 kg/m(2))] performed 30 min of continuous submaximal aerobic 
      exercise at 75% maximal oxygen consumption. Our analyses showed that the BDNF 
      response to acute aerobic exercise was similar in obese and normal-weight 
      subjects across time (time: P = 0.015; group: P = not significant) and was not 
      associated with indices of IR. Although no differences in the rates of CHOoxi and 
      FAToxi were found between both groups, total relative energy expenditure was 
      significantly lower in obese subjects compared to normal-weight subjects (3.53 +/- 
      0.25 versus 5.59 +/- 0.85; P < 0.001). These findings suggest that acute 
      exercise-elicited BDNF elevation may not be sufficient to modulate indices of IR 
      or the utilization of either carbohydrates or fats in obese individuals.
CI  - (c) 2015 British Society for Neuroendocrinology.
FAU - Slusher, A L
AU  - Slusher AL
AD  - Department of Exercise Science and Health Promotion, Florida Atlantic University, 
      Boca Raton, FL, USA; Department of Kinesiology and Health Sciences, Virginia 
      Commonwealth University, Richmond, VA, USA.
FAU - Whitehurst, M
AU  - Whitehurst M
FAU - Zoeller, R F
AU  - Zoeller RF
FAU - Mock, J T
AU  - Mock JT
FAU - Maharaj, A
AU  - Maharaj A
FAU - Huang, C-J
AU  - Huang CJ
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Neuroendocrinol
JT  - Journal of neuroendocrinology
JID - 8913461
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Fats)
RN  - 7171WSG8A2 (BDNF protein, human)
SB  - IM
MH  - Brain-Derived Neurotrophic Factor/blood/*metabolism
MH  - Carbohydrate Metabolism
MH  - Case-Control Studies
MH  - Energy Metabolism/physiology
MH  - Exercise/*physiology
MH  - Fats/metabolism
MH  - Female
MH  - Humans
MH  - Insulin Resistance
MH  - Male
MH  - Obesity/blood/*metabolism
MH  - Oxidation-Reduction
MH  - Oxygen Consumption
MH  - Young Adult
OTO - NOTNLM
OT  - BDNF
OT  - carbohydrate oxidation
OT  - cardiorespiratory fitness
OT  - energy metabolism
OT  - fat oxidation
OT  - insulin resistance
EDAT- 2015/03/17 06:00
MHDA- 2016/02/27 06:00
CRDT- 2015/03/17 06:00
PHST- 2014/11/24 00:00 [received]
PHST- 2015/02/24 00:00 [revised]
PHST- 2015/03/08 00:00 [accepted]
PHST- 2015/03/17 06:00 [entrez]
PHST- 2015/03/17 06:00 [pubmed]
PHST- 2016/02/27 06:00 [medline]
AID - 10.1111/jne.12275 [doi]
PST - ppublish
SO  - J Neuroendocrinol. 2015 May;27(5):370-6. doi: 10.1111/jne.12275.