Literature DB >> 14676847

Persistence of abnormal neural responses to a meal in postobese individuals.

A DelParigi1, K Chen, A D Salbe, J O Hill, R R Wing, E M Reiman, P A Tataranni.   

Abstract

OBJECTIVE: To determine whether abnormal obese-like neural responses to a meal persist in postobese individuals, who achieved and maintained a normal body weight despite a past history of severe obesity. DESIGN AND
SUBJECTS: Cross-sectional study of the brain's response to tasting and consuming a satiating meal in 11 postobese (age: 40+/-6 y, body mass index (BMI): 23.6+/-1.9 kg/m(2)), 23 obese (age: 29+/-6 y, BMI: 39.6+/-3.8 kg/m(2)) and 21 lean (age: 33+/-9 y, BMI: 22.8+/-2.1 kg/m(2)) subjects. MEASUREMENTS: Regional cerebral blood flow (rCBF, a marker of neural activity) at baseline (after a 36-h fast), after tasting and after consuming a satiating liquid meal was assessed using positron emission tomography and state-dependent changes (taste-baseline; satiation-baseline), and compared across groups. Subjective ratings of hunger and fullness were measured by a visual analogue scale and body fatness by dual-energy X-ray absorptiometry.
RESULTS: In response to tasting the liquid meal, changes in rCBF were different in the obese as compared to the lean individuals (P<0.05, corrected for multiple comparisons) in the middle insula (peak voxel, x=-41, y=1, z=8; Montreal Neurological Institute coordinates) and posterior cingulate cortex (peak voxel, x=17, y=-47, z=40). The middle insular cortex exhibited a similar increase of neural activity in the obese and postobese subjects, whereas in the lean subjects the regional activity did not change. In the posterior cingulate cortex, the changes in rCBF in the postobese subjects were not different from those in the other groups. In response to a satiating amount of the same liquid meal, changes in rCBF were different in the obese as compared to the lean individuals (P<0.05, corrected for multiple comparisons) in the posterior hippocampus (peak voxel, x=21, y=-45, x=4), posterior cingulate cortex (peak voxel, x=17, y=-47, z=40), and amygdala (peak voxel, x=27, y=1, z=-24). The posterior hippocampus exhibited a similar decrease of neural activity in the obese and postobese subjects, whereas in the lean subjects the regional activity increased. In the posterior cingulate cortex and amygdala, the changes in rCBF were not different between the postobese and lean individuals. None of the changes in neural activity were correlated with the age of the individuals, the subjective ratings of hunger and fullness, or the meal induced-changes in plasma glucose, insulin, or serum free fatty acids.
CONCLUSION: Persistence of abnormal neural responses to a meal in the postobese individuals, a group at high risk for relapse, indicates that a predisposition to obesity may involve areas of the brain that control complex aspects of eating behavior including anticipation and reward, chemosensory perception, and autonomic control of digestion (insular cortex), as well as enteroception and learning/memory (hippocampus).

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Year:  2004        PMID: 14676847     DOI: 10.1038/sj.ijo.0802558

Source DB:  PubMed          Journal:  Int J Obes Relat Metab Disord


  66 in total

1.  Altered default network activity in obesity.

Authors:  Jason R Tregellas; Korey P Wylie; Donald C Rojas; Jody Tanabe; Jesse Martin; Eugene Kronberg; Dietmar Cordes; Marc-Andre Cornier
Journal:  Obesity (Silver Spring)       Date:  2011-06-02       Impact factor: 5.002

Review 2.  Cognitive and neuronal systems underlying obesity.

Authors:  Scott E Kanoski
Journal:  Physiol Behav       Date:  2012-01-12

3.  "The next mouthful will be the best": influence of prevision of the pleasure on the decision of having a second helping of a just eaten food.

Authors:  Piergiuseppe Vinai; Luisa Vinai; Paolo Vinai; Cecilia Bruno; Stacia Studt; Silvia Cardetti; Donatella Masante; Maurizio Speciale
Journal:  Eat Weight Disord       Date:  2015-11-24       Impact factor: 4.652

4.  Eyes are bigger than the stomach: correlation between body mass index, satiety, and prediction of satiety.

Authors:  P Vinai; D Masante; S Cardetti; N Ferrato; P Vallaur; G Carpegna; S Sassaroli; G M Ruggiero
Journal:  Eat Weight Disord       Date:  2009-12       Impact factor: 4.652

Review 5.  Is your brain to blame for weight regain?

Authors:  Marc-Andre Cornier
Journal:  Physiol Behav       Date:  2011-04-09

Review 6.  A potential role for the hippocampus in energy intake and body weight regulation.

Authors:  Terry L Davidson; Scott E Kanoski; Lindsey A Schier; Deborah J Clegg; Stephen C Benoit
Journal:  Curr Opin Pharmacol       Date:  2007-11-26       Impact factor: 5.547

7.  Orosensory and Homeostatic Functions of the Insular Taste Cortex.

Authors:  Ivan E de Araujo; Paul Geha; Dana M Small
Journal:  Chemosens Percept       Date:  2012-03-01       Impact factor: 1.833

8.  Less activation in the left dorsolateral prefrontal cortex in the reanalysis of the response to a meal in obese than in lean women and its association with successful weight loss.

Authors:  Duc Son Nt Le; Nicola Pannacciulli; Kewei Chen; Arline D Salbe; Angelo Del Parigi; James O Hill; Rena R Wing; Eric M Reiman; Jonathan Krakoff
Journal:  Am J Clin Nutr       Date:  2007-09       Impact factor: 7.045

Review 9.  Comparing the effects of food restriction and overeating on brain reward systems.

Authors:  Nicole M Avena; Susan Murray; Mark S Gold
Journal:  Exp Gerontol       Date:  2013-03-25       Impact factor: 4.032

10.  Midbrain response to milkshake correlates with ad libitum milkshake intake in the absence of hunger.

Authors:  Sarah Nolan-Poupart; Maria G Veldhuizen; Paul Geha; Dana M Small
Journal:  Appetite       Date:  2012-10-12       Impact factor: 3.868

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