Document Detail

PYY modulation of cortical and hypothalamic brain areas predicts feeding behaviour in humans.
MedLine Citation:
PMID:  17934448     Owner:  NLM     Status:  MEDLINE    
The ability to maintain adequate nutrient intake is critical for survival. Complex interrelated neuronal circuits have developed in the mammalian brain to regulate many aspects of feeding behaviour, from food-seeking to meal termination. The hypothalamus and brainstem are thought to be the principal homeostatic brain areas responsible for regulating body weight. However, in the current 'obesogenic' human environment food intake is largely determined by non-homeostatic factors including cognition, emotion and reward, which are primarily processed in corticolimbic and higher cortical brain regions. Although the pleasure of eating is modulated by satiety and food deprivation increases the reward value of food, there is currently no adequate neurobiological account of this interaction between homeostatic and higher centres in the regulation of food intake in humans. Here we show, using functional magnetic resonance imaging, that peptide YY3-36 (PYY), a physiological gut-derived satiety signal, modulates neural activity within both corticolimbic and higher-cortical areas as well as homeostatic brain regions. Under conditions of high plasma PYY concentrations, mimicking the fed state, changes in neural activity within the caudolateral orbital frontal cortex predict feeding behaviour independently of meal-related sensory experiences. In contrast, in conditions of low levels of PYY, hypothalamic activation predicts food intake. Thus, the presence of a postprandial satiety factor switches food intake regulation from a homeostatic to a hedonic, corticolimbic area. Our studies give insights into the neural networks in humans that respond to a specific satiety signal to regulate food intake. An increased understanding of how such homeostatic and higher brain functions are integrated may pave the way for the development of new treatment strategies for obesity.
Rachel L Batterham; Dominic H ffytche; J Miranda Rosenthal; Fernando O Zelaya; Gareth J Barker; Dominic J Withers; Steven C R Williams
Related Documents :
17544318 - Ghrelin: a new peptide regulating growth hormone release and food intake.
15723758 - Neuropeptide y, alpha-melanocyte-stimulating hormone, and monoamines in food intake reg...
9802438 - Neuropeptide y y1 receptor antisense oligodeoxynucleotides enhance food intake in energ...
15936698 - Structure, distribution and physiological functions of ghrelin in fish.
23939268 - Influence of previous experience on the preference, food utilization and performance of...
9972188 - Water: an essential but overlooked nutrient.
Publication Detail:
Type:  Journal Article; Randomized Controlled Trial     Date:  2007-10-14
Journal Detail:
Title:  Nature     Volume:  450     ISSN:  1476-4687     ISO Abbreviation:  Nature     Publication Date:  2007 Nov 
Date Detail:
Created Date:  2007-11-01     Completed Date:  2007-11-28     Revised Date:  2014-02-19    
Medline Journal Info:
Nlm Unique ID:  0410462     Medline TA:  Nature     Country:  England    
Other Details:
Languages:  eng     Pagination:  106-9     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Appetite Regulation / drug effects*,  physiology
Cerebral Cortex / anatomy & histology,  drug effects*,  physiology*
Cross-Over Studies
Feeding Behavior / drug effects*,  physiology
Homeostasis / drug effects
Hypothalamus / drug effects*,  physiology*
Peptide YY / blood,  metabolism,  pharmacology*
Satiation / drug effects,  physiology
Grant Support
G108/551//Medical Research Council
Reg. No./Substance:
106388-42-5/Peptide YY
Comment In:
Cell Metab. 2007 Dec;6(6):423-5   [PMID:  18054310 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  High-resolution structure prediction and the crystallographic phase problem.
Next Document:  Identification of stem cells in small intestine and colon by marker gene Lgr5.