PMID- 22712064
OWN - NLM
STAT- MEDLINE
DCOM- 20120913
LR  - 20240317
IS  - 1873-507X (Electronic)
IS  - 0031-9384 (Print)
IS  - 0031-9384 (Linking)
VI  - 106
IP  - 3
DP  - 2012 Jun 6
TI  - Early postnatal overnutrition: potential roles of gastrointestinal vagal 
      afferents and brain-derived neurotrophic factor.
PG  - 400-12
AB  - Abnormal perinatal nutrition (APN) results in a predisposition to develop obesity 
      and the metabolic syndrome and thus may contribute to the prevalence of these 
      disorders. Obesity, including that which develops in organisms exposed to APN, 
      has been associated with increased meal size. Vagal afferents of the 
      gastrointestinal (GI) tract contribute to regulation of meal size by transmitting 
      satiation signals from gut-to-brain. Consequently, APN could increase meal size 
      by altering this signaling, possibly through changes in expression of factors 
      that control vagal afferent development or function. Here two studies that 
      addressed these possibilities are reviewed. First, meal patterns, meal 
      microstructure, and the structure and density of vagal afferents that innervate 
      the intestine were examined in mice that experienced early postnatal 
      overnutrition (EPO). These studies provided little evidence for EPO effects on 
      vagal afferents as it did not alter meal size or vagal afferent density or 
      structure. However, these mice exhibited modest hyperphagia due to a satiety 
      deficit. In parallel, the possibility that brain-derived neurotrophic factor 
      (BDNF) could mediate APN effects on vagal afferent development was investigated. 
      Brain-derived neurotrophic factor was a strong candidate because APN alters BDNF 
      levels in some tissues and BDNF knockout disrupts development of vagal sensory 
      innervation of the GI tract. Surprisingly, smooth muscle-specific BDNF knockout 
      resulted in early-onset obesity and hyperphagia due to increases in meal size and 
      frequency. Microstructure analysis revealed decreased decay of intake rate during 
      a meal in knockouts, suggesting that the loss of vagal negative feedback 
      contributed to their increase in meal size. However, meal-induced c-Fos 
      activation within the dorsal vagal complex suggested this effect could be due to 
      augmentation of vago-vagal reflexes. A model is proposed to explain how high-fat 
      diet consumption produces increased obesity in organisms exposed to APN, and may 
      be required to reveal effects of EPO on vagal function.
FAU - Fox, Edward A
AU  - Fox EA
AD  - Behavioral Neurogenetics Laboratory & Ingestive Behavior Research Center, 
      Department of Psychological Sciences, Purdue University, West Lafayette, IN 
      47907, USA. au_gc@psych.purdue.edu
FAU - Biddinger, Jessica E
AU  - Biddinger JE
LA  - eng
GR  - R01 NS046716/NS/NINDS NIH HHS/United States
GR  - R01 NS046716-05/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Physiol Behav
JT  - Physiology & behavior
JID - 0151504
RN  - 0 (Brain-Derived Neurotrophic Factor)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Gastrointestinal Tract/*physiopathology
MH  - Humans
MH  - Mice
MH  - Overnutrition/*physiopathology
MH  - *Vagus Nerve
PMC - PMC3517218
MID - NIHMS369516
EDAT- 2012/06/20 06:00
MHDA- 2012/09/14 06:00
PMCR- 2013/06/06
CRDT- 2012/06/20 06:00
PHST- 2012/06/20 06:00 [entrez]
PHST- 2012/06/20 06:00 [pubmed]
PHST- 2012/09/14 06:00 [medline]
PHST- 2013/06/06 00:00 [pmc-release]
AID - S0031-9384(12)00143-6 [pii]
AID - 10.1016/j.physbeh.2012.04.002 [doi]
PST - ppublish
SO  - Physiol Behav. 2012 Jun 6;106(3):400-12. doi: 10.1016/j.physbeh.2012.04.002.