Obese children show hyperactivation to food pictures in brain networks linked to motivation, reward and cognitive control.

Department of Preventive Medicine, Hoglund Brain Imaging Center, The University of Kansas Medical Center, Kansas City, KS, USA.
International journal of obesity (2005) (Impact Factor: 5.22). 05/2010; 34(10):1494-500. DOI: 10.1038/ijo.2010.84
Source: PubMed

ABSTRACT To investigate the neural mechanisms of food motivation in children and adolescents, and examine brain activation differences between healthy weight (HW) and obese participants.
Ten HW children (ages 11-16; BMI < 85%ile) and 10 obese children (ages 10-17; BMI >95%ile) matched for age, gender and years of education.
Functional magnetic resonance imaging (fMRI) scans were conducted twice: when participants were hungry (pre-meal) and immediately after a standardized meal (post-meal). During the fMRI scans, the participants passively viewed blocked images of food, non-food (animals) and blurred baseline control.
Both groups of children showed brain activation to food images in the limbic and paralimbic regions (PFC/OFC). The obese group showed significantly greater activation to food pictures in the PFC (pre-meal) and OFC (post-meal) than the HW group. In addition, the obese group showed less post-meal reduction of activation (vs pre-meal) in the PFC, limbic and the reward-processing regions, including the nucleus accumbens.
Limbic and paralimbic activation in high food motivation states was noted in both groups of participants. However, obese children were hyper-responsive to food stimuli as compared with HW children. In addition, unlike HW children, brain activations in response to food stimuli in obese children failed to diminish significantly after eating. This study provides initial evidence that obesity, even among children, is associated with abnormalities in neural networks involved in food motivation, and that the origins of neural circuitry dysfunction associated with obesity may begin early in life.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Studies in rodents have demonstrated that insulin in the central nervous system induces satiety. In humans, these effects are less well established. Insulin detemir is a basal insulin analog that causes less weight gain than other basal insulin formulations, including the current standard intermediate-long acting Neutral Protamine Hagedorn (NPH) insulin. Due to its structural modifications, which render the molecule more lipophilic, it was proposed that insulin detemir enters the brain more readily than other insulins. The aim of this study was to investigate whether insulin detemir treatment differentially modifies brain activation in response to food stimuli as compared to NPH insulin. In addition, cerebral spinal fluid (CSF) insulin levels were measured after both treatments. Brain responses to viewing food and non-food pictures were measured using functional Magnetic Resonance Imaging in 32 type 1 diabetic patients, after each of two 12-week treatment periods with insulin detemir and NPH insulin, respectively, both combined with prandial insulin aspart. CSF insulin levels were determined in a subgroup. Insulin detemir decreased body weight by 0.8 kg and NPH insulin increased weight by 0.5 kg (p = 0.02 for difference), while both treatments resulted in similar glycemic control. After treatment with insulin detemir, as compared to NPH insulin, brain activation was significantly lower in bilateral insula in response to visual food stimuli, compared to NPH (p = 0.02 for right and p = 0.05 for left insula). Also, CSF insulin levels were higher compared to those with NPH insulin treatment (p = 0.003). Our findings support the hypothesis that in type 1 diabetic patients, the weight sparing effect of insulin detemir may be mediated by its enhanced action on the central nervous system, resulting in blunted activation in bilateral insula, an appetite-regulating brain region, in response to food stimuli. NCT00626080.
    PLoS ONE 01/2014; 9(4):e94483. · 3.73 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: SUMMARY Pediatric-onset multiple sclerosis is relatively rare and research regarding disease characteristics is in its infancy. Regardless, there are a growing number of studies finding early cognitive deficits in this population. There are some similarities in outcomes to those seen in the adult-onset multiple sclerosis population, but also several important differences. With specific regard to cognitive functioning in pediatric-onset multiple sclerosis, there is evidence of deficit in nearly a third of patients, with impairment primarily in areas of processing speed, visual-spatial processing and language. There are additional findings of fatigue and depression that impact functional outcomes requiring further attention in assessment and treatment considerations. This paper also explores other areas requiring increased focus, including treatment and outcomes, neuroimaging and additional disease-modifying factors (comorbidities, socioeconomic status, race and so on).
    Neurodegenerative disease management. 04/2014; 4(2):137-46.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Adequate energy intake is vital for the survival of humans and is regulated by complex homeostatic and hedonic mechanisms. Supported by functional MRI (fMRI) studies that consistently demonstrate differences in brain response as a function of weight status during exposure to appetizing food stimuli, it has been posited that hedonically driven food intake contributes to weight gain and obesity maintenance. These food reward theories of obesity are reliant on the notion that the aberrant brain response to food stimuli relates directly to ingestive behavior, specifically, excess food intake. Importantly, functioning of homeostatic neuroendocrine regulators of food intake, such as leptin and ghrelin, are impacted by weight status. Thus, data from studies that evaluate the effect on weight status on brain response to food may be a result of differences in neuroendocrine functioning and/or behavior. In the present review, we examine the influence of weight and weight change, exogenous administration of appetitive hormones, and ingestive behavior on BOLD response to food stimuli.
    Physiology & Behavior 04/2014; · 3.16 Impact Factor

Full-text (2 Sources)

Available from
May 22, 2014

Similar Publications