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Specific white matter tissue microstructure changes associated with obesity

Stephanie Kullmann, Martina F. Callaghan, Martin Heni, Nikolaus Weiskopf, Klaus Scheffler, Hans-Ulrich Häring, Andreas Fritsche, Ralf Veit, Hubert Preissl

NeuroImage 125 (2016) 36–44

Obesity-related structural brain alterations point to a consistent reduction in gray matter with increasing body mass index (BMI) but changes in white matter have proven to be more complex and less conclusive. Hence, more recently diffusion tensor imaging (DTI) has been employed to investigate microstructural changes in white matter structure. Altogether, these studies have mostly shown a loss of white matter integrity with obesity-related factors in several brain regions. However, the variety of these obesity-related factors, including inflammation and dyslipidemia, resulted in competing influences on the DTI indices. To increase the specificity of DTI results, we explored specific brain tissue properties by combining DTI with quantitative multiparameter mapping in lean, overweight and obese young adults. By means of multi-parameter mapping, white matter structures showed differences in MRI parameters consistent with reduced myelin, increased water and altered iron contentwith increasing BMI in the superior longitudinal fasciculus, anterior thalamic radiation, internal
capsule and corpus callosum. BMI-related changes in DTI parameters revealedmainly alterations inmean and axial diffusivity with increasing BMI in the corticospinal tract, anterior thalamic radiation and superior longitudinal fasciculus. These alterations, including mainly fiber tracts linking limbic structures with prefrontal regions, could potentially promote accelerated aging in obese individuals leading to an increased risk for cognitive decline.

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Ghrelin Regulates Glucose and Glutamate Transporters in Hypothalamic Astrocytes

Esther Fuente-Martín, Cristina García-Cáceres, Pilar Argente-Arizón, Francisca Díaz, Miriam Granado, Alejandra Freire-Regatillo, David Castro-González, María L. Ceballos, Laura M. Frago, Suzanne L. Dickson, Jesús Argente & Julie A. Chowen

Scientific Reports 6 2016

Hypothalamic astrocytes can respond to metabolic signals, such as leptin and insulin, to modulate adjacent neuronal circuits and systemic metabolism. Ghrelin regulates appetite, adiposity and glucose metabolism, but little is known regarding the response of astrocytes to this orexigenic hormone. We
have used both in vivo and in vitro approaches to demonstrate that acylated ghrelin (acyl-ghrelin) rapidly stimulates glutamate transporter expression and glutamate uptake by astrocytes. Moreover, acyl-ghrelin rapidly reduces glucose transporter (GLUT) 2 levels and glucose uptake by these glial cells. Glutamine synthetase and lactate dehydrogenase decrease, while glycogen phosphorylase and lactate transporters increase in response to acyl-ghrelin, suggesting a change in glutamate and glucose metabolism, as well as glycogen storage by astrocytes. These effects are partially mediated through
ghrelin receptor 1A (GHSR-1A) as astrocytes do not respond equally to desacyl-ghrelin, an isoform that does not activate GHSR-1A. Moreover, primary astrocyte cultures from GHSR-1A knock-out mice do not change glutamate transporter or GLUT2 levels in response to acyl-ghrelin. Our results indicate that acylghrelin may mediate part of its metabolic actions through modulation of hypothalamic astrocytes and that this effect could involve astrocyte mediated changes in local glucose and glutamate metabolism that alter the signals/nutrients reaching neighboring neurons.

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The Stomach-Derived Hormone Ghrelin Increases Impulsive Behavior

Rozita H Anderberg, Caroline Hansson, Maya Fenander, Jennifer E Richard, Suzanne L Dickson,
Hans Nissbrandt, Filip Bergquist and Karolina P Skibicka

Neuropsychopharmacology (2016) 41, 1199–1209


Impulsivity, defined as impaired decision making, is associated with many psychiatric and behavioral disorders, such as attention-deficit/ hyperactivity disorder as well as eating disorders. Recent data indicate that there is a strong positive correlation between food reward behavior and impulsivity, but the mechanisms behind this relationship remain unknown. Here we hypothesize that ghrelin, an orexigenic hormone produced by the stomach and known to increase food reward behavior, also increases impulsivity. In order to assess the impactof ghrelin on impulsivity, rats were trained in three complementary tests of impulsive behavior and choice: differential reinforcement of lowrate (DRL), go/no-go, and delay discounting. Ghrelin injection into the lateral ventricle increased impulsive behavior, as indicated by reduced efficiency of performance in the DRL test, and increased lever pressing during the no-go periods of the go/no-go test. Central ghrelin stimulation also increased impulsive choice, as evidenced by the reduced choice for large rewards when delivered with a delay in the delay discounting test. In order to determine whether signaling at the central ghrelin receptors is necessary for maintenance of normal levels of impulsive behavior, DRL performance was assessed following ghrelin receptor blockade with central infusion of a ghrelin receptor antagonist. Central ghrelin receptor blockade reduced impulsive behavior, as reflected by increased efficiency of performance in the DRL task. To further investigate the neurobiological substrate underlying the impulsivity effect of ghrelin, we microinjected ghrelin into the ventral tegmental area, an area harboring dopaminergic cell bodies. Ghrelin receptor stimulation within the VTA was sufficient to increase impulsive behavior. We further evaluated the impact of ghrelin on dopamine-related gene expression and dopamine turnover in brain areas key in impulsive behavior control. This study provides the first demonstration that the stomach-produced hormone ghrelin increases impulsivity and also indicates that ghrelin can change two major components of impulsivity—motor and choice impulsivity.

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Effects of eating rate on satiety: A role for episodic memory?

Danielle Ferriday, Matthew L. Bosworth, Samantha Lai, Nicolas Godinot, Nathalie Martin, Ashley A. Martin, Peter J. Rogers, Jeffrey M. Brunstrom

Physiology & Behavior 152 (2015) 389–396

Eating slowly is associated with a lower body mass index. However, the underlying mechanism is poorly understood. Here, our objective was to determinewhether eating a meal at a slow rate improves episodic memory for the meal and promotes satiety. Participants (N=40) consumed a 400 ml portion of tomato soup at either a fast (1.97 ml/s) or a slow (0.50 ml/s) rate. Appetite ratings were elicited at baseline and at the end of the meal
(satiation). Satiety was assessed using; i) an ad libitum biscuit ‘taste test’ (3 h after the meal) and ii) appetite ratings (collected 2 h after the meal and after the ad libitum snack). Finally, to evaluate episodic memory for the meal, participants self-served the volume of soup that they believed they had consumed earlier (portion size memory) and completed a rating of memory ‘vividness’. Participantswho consumed the soup slowly reported a greater increase in fullness, both at the end of the meal and during the inter-meal interval. However, we found little effect of eating rate on subsequent ad libitum snack intake. Importantly, after 3 h, participants who ate the soup slowly remembered eating a larger portion. These findings show that eating slowly promotes
self-reported satiation and satiety. For the first time, they also suggest that eating rate influences portion size memory. However, eating slowly did not affect ratings of memory vividness and we found little evidence for a relationship between episodic memory and satiety. Therefore, we are unable to conclude that episodic memory mediates effects of eating rate on satiety.

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Empty calories and phantom fullness: a randomized trial studying the relative effects of energy density and viscosity on gastric emptying determined by MRI and satiety

Guido Camps, Monica Mars, Cees de Graaf, and Paul AM Smeets

American Journal of Clinical Nutrition 2016;104:1-8

In recently published work from the Nudge-it team at Wageningen University we have shown that fullness isn't the same as being full.

Being full is less affected by how full your stomach  is, but more by the the taste and feeling in your mouth of what you've eaten. This leaves us to conclude that thin liquids may leave you feeling rather empty, regardless of their caloric load (in our case a respectable 500Kcal). The opposite is true of a thick, slow to drink, 100Kcal shake, which left the stomach quickly, but also left the drinker feeling rather fuller.

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Subtypes of trait impulsivity differentially correlate with neural responses to food choices

Laura N. van der Laan,  E.A. Barendse, Max A. Viergever, Paul A.M. Smeets

Behavioural Brain Research Volume 296, 1 January 2016, Pages 442–450

Impulsivity is a personality trait that is linked to unhealthy eating and overweight. A few studies assessed how impulsivity relates to neural responses to anticipating and tasting food, but it is unknown how impulsivity relates to neural responses during food choice. Although impulsivity is a multi-faceted construct, it is unknown whether impulsivity subtypes have different underlying neural mechanisms. We investigated how impulsivity correlates with brain responses during food choice and in how far different impulsivity subtypes modulate brain responses during food choice differently. Twenty weight-concerned females performed an fMRI task in which they indicated for high and low energy snacks whether or not they wanted to eat them. Impulsivity subtypes were measured by the monetary delay discounting task and the Barratt Impulsiveness Scale (total BIS-11 and subscales). Only temporal subtypes of impulsivity, namely delay discounting and the BIS-11 non-planning subscale, modulated responses to food choice; both measures correlated positively with striatum activation during high versus low energy choices. However, only delay discounting predicted high energy choices, whereas BIS-11 non-planning independently related to a striatum region that reflects subjective stimulus value. To conclude, the brain mechanisms underlying subtypes of impulsivity have a common ground but differ in specific aspects of food-related decision-making. The findings advance our understanding of the neural correlates of different impulsivity subtypes in the food domain.

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Supersize my brain: A cross-sectional voxel-based morphometrystudy on the association between self-reported dietary restraint andregional grey matter volumes

Laura N. van der Laan,Lisette Charbonnier, Sanne Griffioen-Roose, Floor M. Kroese, Inge van Rijn, Paul A.M. Smeets,

Biological Psychology 117 (2016) 108–116

Restrained eaters do not eat less than their unrestrained counterparts. Proposed underlying mechanismsare that restrained eaters are more reward sensitive and that they have worse inhibitory control. AlthoughfMRI studies assessed these mechanisms, it is unknown how brain anatomy relates to dietary restraint.Voxel-based morphometry was performed on anatomical scans from 155 normal-weight females toinvestigate how regional grey matter volume correlates with restraint. A positive correlation was foundin several areas, including the parahippocampal gyrus, hippocampus, striatum and the amygdala (bilat-erally, p < 0.05, corrected). A negative correlation was found in several areas, including the inferior frontalgyrus, superior frontal gyrus, supplementary motor area, middle cingulate cortex and precentral gyrus(p < 0.05, corrected). That higher restraint relates to higher grey matter volume in reward-related areasand lower grey matter volume in regions involved in inhibition, provides a neuroanatomical underpinningof theories relating restraint to increased reward sensitivity and reduced inhibitory capacity.

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Dopamine Depletion Reduces Food-Related Reward Activity Independent of BMI

Sabine Frank, Ralf Veit, Helene Sauer, Paul Enck, Hans-Christoph Friederich, Theresa Unholzer, Ute-Maria Bauer, Katarzyna Linder, Martin Heni

Andreas Fritsche and Hubert Preissl

Neuropsychopharmacology (2015), 1–9

Reward sensitivity and possible alterations in the dopaminergic-reward system are associated with obesity. We therefore aimed to investigate the influence of dopamine depletion on food-reward processing. We investigated 34 female subjects in a randomized placebocontrolled, within-subject design (body mass index (BMI)=27.0 kg/m2 ±4.79 SD; age=28 years ±4.97 SD) using an acute phenylalanine/tyrosine depletion drink representing dopamine depletion and a balanced amino acid drink as the control condition. Brain activity was measured with functional magnetic resonance imaging during a ‘wanting’ and ‘liking’ rating of food items. Eating behavior-related traits and states were assessed on the basis of questionnaires. Dopamine depletion resulted in reduced activation in the striatum and higher activation in the superior frontal gyrus independent of BMI. Brain activity during the wanting task activated a more distributed network than during the liking task.


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Selective Insulin Resistance in Homeostatic and Cognitive Control Brain Areas in Overweight and Obese Adults

Stephanie Kullmann, Martin Heni, Ralf Veit, Klaus Scheffler, Jurgen Machann, Hans-Ulrich Haring,
Andreas Fritsche, and Hubert Preissl

Diabetes Care 2015;38:1044–1050

Due to strong associations with numerous conditions, such as type 2 diabetes and cardiovascular disease, obesity has become a major public health concern. Obesity is associated with peripheral insulin resistance in many organs, such as muscle, liver, and adipose tissue. However, only recently was the brain identified as an insulinsensitive organ regulating food intake. In humans, the central nervous effects of insulin still remain ill defined. In search of new insights in the pathogenesis of obesity and brain insulin resistance, modern neuroimaging techniques have emerged as valuable tools to investigate insulin action in the human brain.

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So Many Brands and Varieties to Choose from: Does This Compromise the Control of Food Intake in Humans?

Charlotte A. Hardman, Danielle Ferriday, Lesley Kyle, Peter J. Rogers, and Jeffrey M. Brunstrom

PLoS ONE 10(4):1-17 (2015)

The recent rise in obesity is widely attributed to changes in the dietary environment (e.g., increased availability of energy-dense foods and larger portion sizes). However, a critical feature of our “obesogenic environment” may have been overlooked - the dramatic increase in
“dietary variability” (the tendency for specific mass-produced foods to be available in numerous varieties that differ in energy content). In this study we tested the hypothesis that dietary variability compromises the control of food intake in humans

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