Brain-derived neurotrophic factor, corticotropin-releasing factor, and hypothalamic neuronal histamine interact to regulate feeding behavior

2013 ◽  
Vol 125 (4) ◽  
pp. 588-598 ◽  
Author(s):  
Koro Gotoh ◽  
Takayuki Masaki ◽  
Seiichi Chiba ◽  
Hisae Ando ◽  
Kansuke Fujiwara ◽  
...  
Keyword(s):  
Feeding Behavior ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Corticotropin Releasing Factor ◽  
Neuronal Histamine

scholarly journals Increased Food Intake Leads to Obesity and Insulin Resistance in the Tg2576 Alzheimer’s Disease Mouse Model

Endocrinology ◽  
2010 ◽  
Vol 151 (4) ◽  
pp. 1532-1540 ◽  
Author(s):  
Motoyuki Kohjima ◽  
Yuxiang Sun ◽  
Lawrence Chan
Keyword(s):  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Food Intake ◽  
Mouse Model ◽  
Feeding Behavior ◽  
Neurotrophic Factor ◽  
Caloric Intake ◽  
Brain Derived Neurotrophic Factor ◽  
Normal Diet ◽  
The Brain

Recent studies suggest that hyperinsulinemia and insulin resistance are linked to Alzheimer’s disease (AD). In this study, we used Tg2576 transgenic (Tg) mice, a widely used transgenic mouse model for AD, to explore the relationship between increased amyloid β-peptide (Aβ) and insulin resistance. When fed a high-fat diet (HFD), Tg mice developed obesity and insulin resistance at 16 wk of age. Furthermore, HFD-fed Tg mice displayed abnormal feeding behavior and increased caloric intake with time. Although caloric intake of HFD-fed Tg mice was similar to that of normal diet-fed Tg or wild-type mice during 4 to 8 wk of age, it increased sharply at 12 wk, and went up further at 16 wk, which paralleled changes in the level of Aβ40 and Aβ42 in the brain of these mice. Limiting food intake in HFD-fed Tg mice by pair-feeding a caloric intake identical with that of normal diet-fed mice completely prevented the obesity and insulin intolerance of HFD-fed Tg mice. The hypothalamus of HFD-fed Tg mice had a significant decrease in the expression of the anorexigenic neuropeptide, brain-derived neurotrophic factor, at both the mRNA and protein levels. These findings suggest that the increased Aβ in the brain of HFD-fed Tg2576 mice is associated with reduced brain-derived neurotrophic factor expression, which led to abnormal feeding behavior and increased food intake, resulting in obesity and insulin resistance in these animals.

Brain-derived neurotrophic factor in the ventromedial nucleus of the hypothalamus reduces energy intake

2007 ◽  
Vol 293 (3) ◽  
pp. R1037-R1045 ◽  
Author(s):  
ChuanFeng Wang ◽  
Eric Bomberg ◽  
Allen Levine ◽  
Charles Billington ◽  
Catherine M. Kotz
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Feeding Behavior ◽  
Neurotrophic Factor ◽  
Body Weight Gain ◽  
Brain Derived Neurotrophic Factor ◽  
Brain Regions ◽  
Ventromedial Nucleus ◽  
Bdnf Mrna ◽  
Site Of Action

Recent studies show that brain-derived neurotrophic factor (BDNF) decreases feeding and body weight after peripheral and ventricular administration. BDNF mRNA and protein, and its receptor TrkB, are widely distributed in the hypothalamus and other brain regions. However, there are few reports on specific brain sites of actions for BDNF. We evaluated the effect of BDNF, given into the ventromedial nucleus of the hypothalamus (VMH), on normal and deprivation- and neuropeptide Y (NPY)-induced feeding behavior and body weight. BDNF injected unilaterally or bilaterally into the VMH of food-deprived and nondeprived rats significantly decreased feeding and body weight gain within the 0- to 24-h and the 24- to 48-h postinjection intervals. Doses effectively producing inhibition of feeding behavior did not establish a conditioned taste aversion. BDNF-induced feeding inhibition was attenuated by pretreatment of the TrkB-Fc fusion protein that blocks binding between BDNF and its receptor TrkB. VMH-injected BDNF significantly decreased VMH NPY-induced feeding at 1, 2, and 4 h after injection. In summary, BDNF in the VMH significantly decreases food intake and body weight gain, by TrkB receptor-mediated actions. Furthermore, the anorectic effects of BDNF in this site appear to be mediated by NPY. These data suggest that the VMH is an important site of action for BDNF in its effects on energy metabolism.

Effects of β-Adrenoreceptor Blockade During Chronic Exercise on Contextual Fear Conditioning and mRNA for Galanin and Brain-Derived Neurotrophic Factor.

2004 ◽  
Vol 118 (6) ◽  
pp. 1378-1390 ◽  
Author(s):  
Jacqueline D. Van Hoomissen ◽  
Philip V. Holmes ◽  
Andrew S. Zellner ◽  
Adeline Poudevigne ◽  
Rod K. Dishman
Keyword(s):  
Fear Conditioning ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Contextual Fear Conditioning ◽  
Chronic Exercise ◽  
Contextual Fear

Brain Derived Neurotrophic Factor Gene Polymorphism Associated With Language Acquisition

2007 ◽  
Author(s):  
Scott H. Fraundorf ◽  
Brad E. Sheese ◽  
Lauren K. White ◽  
Mary K. Rothbart ◽  
Michael I. Posner
Keyword(s):  
Language Acquisition ◽  
Gene Polymorphism ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Factor Gene

Brain-derived neurotrophic factor plasma levels in patients suffering from post-traumatic stress disorder

2009 ◽  
Author(s):  
L. Dell'osso ◽  
C. Carmassi ◽  
A. Del Debbio ◽  
M. C. Dell'osso ◽  
C. Bianchi ◽  
...  
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Neurotrophic Factor ◽  
Plasma Levels ◽  
Stress Disorder ◽  
Brain Derived Neurotrophic Factor ◽  
Post Traumatic Stress ◽  
Post Traumatic

Von der Entzündung zur Degeneration: die Bedeutung des Neurotrophins brain derived neurotrophic factor bei autoimmuner Entmarkung im zentralen Nervensystem

2008 ◽  
Vol 35 (S 01) ◽  
Author(s):  
F Lühder ◽  
D Lee ◽  
S Cetin ◽  
S Wiese ◽  
N Kruse ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor

Brain derived neurotrophic factor (BDNF) reguliert Apoptose in primärer enterischer Glia über einen autokrinen Mechanismus

2008 ◽  
Vol 46 (09) ◽  
Author(s):  
M Steinkamp ◽  
N Degenkolb ◽  
H Gundel ◽  
S Kunsch ◽  
G Adler ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor
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