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Large Portions Encourage the Selection of Palatable Rather Than Filling Foods

Jeffrey M Brunstrom, Andreas Jarvstad, Rebecca L Griggs, Christina Potter, Natalie R Evans, Ashley A Martin,

Jon CW Brooks, and Peter J Rogers

Journal of Nutriton 2016, 146: 2117-2123

Portion size is an important driver of larger meals. However, effects on food choice remain unclear. Our aim was to identify how portion size influences the effect of palatability and expected satiety on choice.

In study 1 adult participants (n = 24, 87.5% women) evaluated the palatability and expected satiety of 5 lunchtime meals and ranked them in order of preference. Separate ranks were elicited for equicaloric portions from 100 to 800 kcal (100-kcal steps). In study 2, adult participants (n = 24, 75% women) evaluated 9 meals and ranked 100–600 kcal portions in 3 contexts (scenarios), believing that 1) the next meal would be at 1900, 2) they would receive only a bite of one food, and 3) a favorite dish would be offered immediately afterwards. Regression analysis was used to
quantify predictors of choice.

In Study 1, the extent to which expected satiety and palatability predicted choice was highly dependent on
portion size (P < 0.001). With smaller portions, expected satiety was a positive predictor, playing a role equal to palatability (100-kcal portions: expected satiety, b: 0.42; palatability, b: 0.46). With larger portions, palatability was a strong predictor (600-kcal portions: b: 0.53), and expected satiety was a poor or negative predictor (600-kcal portions: b: 20.42).

In Study 2,this pattern was moderated by context (P = 0.024). Results from scenario 1 replicated Study 1. However, expected satietywas a poor predictor in both scenario 2 (expected satiety was irrelevant) and scenario 3 (satiety was guaranteed), and palatability was the primary driver of choice across all portions.

In adults, expected satiety influences food choice, but only when small equicaloric portions are compared. Larger portions not only promote the consumption of larger meals, but they encourage the adoption of food choice strategies motivated solely by palatability

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Oxytocin Neurones: Intrinsic Mechanisms Governing the Regularity of Spiking Activity

J. Maícas Royo, C. H. Brown, G. Leng and D.J.MacGregor

Journal of Neuroendocrinology, 28 10.1111 2016

Oxytocin neurones of the rat supraoptic nucleus are osmoresponsive and, with all other things being equal, they fire at a mean rate that is proportional to the plasma sodium concentration. However, individual spike times are governed by highly stochastic events, namely the random occurrences of excitatory synaptic inputs, the probability of which is increased by increasing extracellular osmotic pressure. Accordingly, interspike intervals (ISIs) are very irregular. In the present study, we show, by statistical analyses of firing patterns in oxytocin neurones, that the mean firing rate as measured in bins of a few seconds is more regular than expected from the variability of ISIs. This is consistent with an intrinsic activity-dependent negative-feedback mechanism. To test this, we compared observed neuronal firing patterns with firing patterns generated by a leaky integrate-and-fire model neurone, modified to exhibit activity-dependent mechanisms known to be present in oxytocin neurones. The presence of a prolonged afterhyperpolarisation (AHP) was critical for the ability to mimic the observed regularisation of mean firing rate, although we also had to add a depolarising afterpotential (DAP; sometimes called an afterdepolarisation) to the model to match the observed ISI distributions. We tested this model by comparing its behaviour with the behaviour of oxytocin neurones exposed to apamin, a blocker of the medium AHP. Good fits indicate that the medium AHP actively contributes to the firing patterns of oxytocin neurones during non-bursting activity, and that oxytocin neurones generally express a DAP, even though this is usually masked by superposition of a larger AHP.

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Centrally Administered Ghrelin Acutely Influences Food Choice in Rodents

Erik Schele, Tina Bake, Cristina Rabasa, Suzanne Dickson

PLOSone February 2016

We sought to determine whether the orexigenic hormone, ghrelin, is involved in the intrinsic regulation of food choice in rats. Ghrelin would seem suited to serve such a role given that it signals hunger information from the stomach to brain areas important for feeding control, including the hypothalamus and reward system (e.g. ventral tegmental area, VTA). Thus, in rats offered a choice of palatable foods (sucrose pellets and lard) superimposed on regular chow for 2 weeks, we explored whether acute central delivery of ghrelin (intracerebroventricular (ICV) or intra-VTA) is able to redirect their dietary choice. The major unexpected finding is that, in rats with high baseline lard intake, acute ICV ghrelin injection increased their chow intake over 3-fold, relative to vehicle-injected controls, measured at both 3 hr and 6 hr after injection. Similar effects were observed when ghrelin was delivered to the VTA, thereby identifying the VTA as a likely contributing neurobiological substrate for these effects. We also explored food choice after an overnight fast, when endogenous ghrelin levels are elevated, and found similar effects of dietary choice to those described for ghrelin. These effects of fasting on food choice were suppressed in models of suppressed ghrelin signaling (i.e. peripheral injection of a ghrelin receptor antagonist to rats and ghrelin receptor (GHSR) knock-out mice), implicating a role for endogenous ghrelin in the changes in food choice that occur after an overnight fast. Thus, in line with its role as a gut-brain hunger hormone, ghrelin appears to be able to acutely alter food choice, with notable effects to promote “healthy” chow intake, and identify the VTA as a likely contributing neurobiological substrate for these effects

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Appetite and energy balancing

Peter J Rodgers and Jeffrey M Brunstrom

Physiology and Behaviour (in Press)

The idea that food intake is motivated by (or in anticipation of) ‘hunger’ arising from energy depletion is apparent in both public and scientific discourse on eating behaviour. In contrast, our thesis is that eating is largely unrelated to short-term energy depletion. Energy requirements meal-to-meal are trivial compared with total body energy stores, and energy supply to the body's tissues is maintained if a meal or even several meals are missed. Complex and exquisite metabolic machinery ensures that this happens, but metabolic regulation is only loosely coupled with the control of energy intake. Instead, food intake needs to be controlled because the limited capacity of the gut means that processing a meal presents a significant physiological challenge and potentially hinders other activities. We illustrate the relationship between energy (food) intake and energy expenditure with a simple analogy in which: (1) water in a bathtub represents body energy content, (2) water in a saucepan represents food in the gut, and (3) the bathtub is filled via the saucepan. Furthermore, (4) it takes hours to process and pass the full energy (macronutrient) content of the saucepan to the bathtub, and (5) both the saucepan and bathtub resist filling, representing negative feedbacks on appetite (desire to eat). This model is consistent with the observations that appetite is reduced acutely by energy intake (a meal added to the limited capacity of the saucepan/gut), but not increased by an acute increase in energy expenditure (energy removed from the large store of energy in the bathtub/body). The existence of relatively very weak but chronic negative feedback on appetite proportional to body fatness is supported by observations on the dynamics of energy intake and weight gain in rat dietary obesity. (We use the term ‘appetite’ here because ‘hunger’ implies energy depletion.) In our model, appetite is motivated by the accessibility of food and the anticipated and experienced pleasure of eating it. The latter, which is similar to food reward, is determined primarily by the state of emptiness of the gut and food liking related to the food's sensory qualities and macronutrient value and the individual's dietary history. Importantly, energy density adds value because energy dense foods are less satiating kJ for kJ and satiation limits further intake. That is, energy dense foods promote energy intake by virtue (1) of being more attractive and (2) having low satiating capacity kJ for kJ, and (1) is partly a consequence of (2). Energy storage is adapted to feast and famine and that includes unevenness over time of the costs of obtaining and ingesting food compared with engaging in other activities. However, in very low-cost food environments with energy dense foods readily available, risk of obesity is high. This risk can be and is mitigated by dietary restraint, which in its simplest form could mean missing the occasional meal. Another strategy we discuss is the energy dilution achieved by replacing some sugar in the diet with low-calorie sweeteners. Perhaps as or more significant, though, is that belief in short-term energy balancing (the energy depletion model) may undermine attempts to eat less. Therefore, correcting narratives of eating to be consistent with biological reality could also assist with weight control.

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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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