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Parental beliefs about portion size, not children’s own beliefs, predict child BMI

C. Potter, D. Ferriday, R. L. Griggs, J. P. Hamilton-Shield, P. J. Rogers and J. M. Brunstrom

Pediatric Obesity 13, 232–238, April 2018


Background:  Increases in portion size are thought by many to promote obesity in children. However, this relationship remains unclear. Here, we explore the extent to which a child’s BMI is predicted both by parental beliefs about their child’s ideal and maximum portion size and/or by the child’s own beliefs.
Methods:  Parent–child (5–11 years) dyads (N = 217) were recruited from a randomized controlled trial (n = 69) and an interactive science centre (n = 148).For a range of main meals, parents estimated their child’s ‘ideal’ and ‘maximum
tolerated’ portions. Children completed the same tasks.
Results:  An association was found between parents’ beliefs about their child’s ideal (β = .34, p < .001) and maximum tolerated (β = .30, p < .001) portions, and their child’s BMI. By contrast, children’s self-reported ideal (β = .02, p = .718) and maximum tolerated (β = .09, p = .214) portions did not predict their BMI. With increasing child BMI, parents’ estimations aligned more closely with their child’s own selected portions.
Conclusions:  Our findings suggest that when a parent selects a smaller portion for their child than their child self-selects, then the child is less likely to be obese. Therefore, public health measures to prevent obesity might include instructions to parents on appropriate portions for young children.

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The association of serum leptin levels with food addiction is moderated by weight status in adolescent psychiatric inpatients

Triinu Peters, Jochen Antel,  Manuel Föcker,  Simon Esber,  Anke Hinney, Erik Schéle, Suzanne L. Dickson,  Özgür Albayrak, Johannes Hebebrand

European Eating Disorders Review. 2018;26:618–628.


Leptin is essential for the control of energy homeostasis and eating behaviour. We investigated potential associations between serum leptin levels and food addiction in adolescent psychiatric inpatients (n = 228). The most frequent psychiatric diagnoses were mood disorders, anxiety disorders, and substance use disorders. More than three quarters of the study group suffered from more than one psychiatric disorder. Food addiction was assessed with the Yale Food Addiction Scale. Leptin was determined in serum. Analyses were conducted for the whole body weight range and for distinct weight categories to evaluate a potential impact of known nonlinearity between leptin levels and satiety due to leptin resistance in obese. A weak negative association between food addiction and leptin in normal weight patients (ß = −0.11, p = .022) was detected. In contrast, food addiction was associated with a significantly higher serum leptin (ß = 0.16. p = .038) in overweight patients. Food addiction in normal weight patients might be associated with restrained eating, previously shown to involve reduced leptin levels. The small positive association of food addiction
with higher serum leptin in overweight patients might reflect leptin resistance and overeating.

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Microbiota in obesity: interactions with enteroendocrine, immune and central nervous systems

R. J. Mulders, K. C. G. de Git, E. Schéle, S. L. Dickson, Y. Sanz and R. A. H. Adan

Obesity Reviews:  Etiology and Pathophysiology

Western diets, with high consumption of simple sugars and saturated fats, contribute to the rise in the prevalence of obesity. It now seems clear that high-fat diets cause obesity, at least in part, by modifying the composition and function of the microorganisms that colonize in the gastrointestinal tract, the microbiota. The exact pathways by which intestinal microbiota contribute to obesity remain largely unknown. High-fat diet-induced alterations in intestinal microbiota have been suggested to increase energy extraction, intestinal permeability and systemic inflammation while decreasing the capability to generate obesity-suppressing short-chain fatty acids. Moreover, by increasing systemic inflammation, microglial activation and affecting vagal nerve activity, ‘obese microbiota’ indirectly influence hypothalamic gene expression and promote overeating. Because the potential of intestinal microbiota to induce obesity has been recognized, multiple ways to modify its composition and function are being investigated to provide novel preventive and therapeutic strategies against diet-induced obesity.

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Licence to eat: Information on energy expended during exercise affects subsequent energy intake

Duncan C. McCaig, Lydia A. Hawkins, Peter J. Rogers

Appetite 107 (2016) 323-329

An acute bout of exercise, compared with no exercise, appears to have little influence on subsequent energy intake (EI), resulting in short-term negative energy balance. Whereas the labelling of food is evidenced to influence EI, little research has focused on how EI is affected by framing acute exercise in different ways. To explore this, 70 healthy, mostly lean, male and female participants in the current study completed a set amount of exercise (estimated energy expenditure (EE) 120 kcal), but were informed on three occasions before and after the exercise that they had expended either 50 kcal or 265 kcal. An ad libitum test meal, comprising orange juice, tortilla chips and chocolate chip cookies, was then presented after a 10-min break to assess subsequent EI. Measures of hunger and dietary restraint were also completed. Greater EI, primarily driven by chocolate chip cookie consumption (p ¼ 0.015), was observed
in participants receiving 265 kcal EE information. Hunger ratings were significantly lower in the 265 kcal EE information group than in the 50 kcal group following the test meal (p ¼ 0.035), but not immediately after the exercise. These results support an interpretation that higher EE information (265 kcal) provides participants with a greater ‘licence to eat’ when palatable foods are accessible. Tentative evidence for a moderating effect of dietary restraint was observed, indicating a greater influence of EE information in participants with lower restraint. The findings of the current study suggest that the provision of EE information (e.g., through mobile device apps) could be counter-productive to healthy
weight management

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Anatomical projections of the dorsomedial hypothalamus to the periaqueductal grey and their role in thermoregulation: a cautionary note

Kathy C. G. de Git, Diana C. van Tuijl, Mieneke C. M. Luijendijk, Inge G. Wolterink-Donselaar, Alexander Ghanem, Karl-Klaus Conzelmann & Roger A. H. Adan

Physiological Reports 2018 | Vol. 6 | Iss. 14 | e13807

The DMH is known to regulate brown adipose tissue (BAT) thermogenesis via projections to sympathetic premotor neurons in the raphe pallidus, but there is evidence that the periaqueductal gray (PAG) is also an important relay
in the descending pathways regulating thermogenesis. The anatomical projections from the DMH to the PAG subdivisions and their function are largely elusive, and may differ per anterior–posterior level from bregma. We here
aimed to investigate the anatomical projections from the DMH to the PAG along the entire anterior–posterior axis of the PAG, and to study the role of these projections in thermogenesis in Wistar rats. Anterograde channel rhodopsin
viral tracing showed that the DMH projects especially to the dorsal and lateral PAG. Retrograde rabies viral tracing confirmed this, but also indicated that the PAG receives a diffuse input from the DMH and adjacent hypothalamic subregions. We aimed to study the role of the identified DMH to PAG projections in thermogenesis in conscious rats by specifically activating them using a combination of canine adenovirus-2 (CAV2Cre) and Credependent
designer receptor exclusively activated by designer drugs (DREADD) technology. Chemogenetic activation of DMH to PAG projections increased BAT temperature and core body temperature, but we cannot exclude the possibility that at least some thermogenic effects were mediated by adjacent hypothalamic subregions due to difficulties in specifically targeting the DMH and distinct subdivisions of the PAG because of diffuse virus expression. To conclude, our study shows the complexity of the anatomical and functional connection between the hypothalamus and the PAG, and some technical challenges in studying their connection.

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Enhancing excitability of dopamine neurons promotes motivational behaviour through increased action initiation

Linde Boekhoudta, Ellen C.Wijbransa, Jodie H.K.Mana, Mieneke C.M.Luijendijka, Johannes Jonga, Geoffrey van der Plasse, LoukJ.M.J.Vanderschuren, Roger A.H.Adan


European Neuropsychopharmacology(2018) 28, 171–184

Motivational deficits are a key symptom in multiple psychiatric disorders, including major depressive disorder,schizophrenia and addiction.A likely neural substrate for these motivational deficits is the brain dopamine(DA) system. In particular ,DA signalling in the nucleus accumbens, which originates from DA neurons in the ventral tegmental area (VTA), has been identified as a crucia lsubstrate for effort-related and activational aspects of motivation.
Unravelling how VTA DA neuronal activity relates to motivational behaviours is required to understand how motivational deficits in psychiatry can be specifically targeted.  In this study, we therefore used designer receptors exclusively activated by designer drugs (DREADD) in TH:Cre rats, in order to determine the effects of chemogenetic DA neuron activation on different aspects of motivational behaviour. We found that chemogenetic activation of DA neurons in the
VTA,but not substantia nigra, significantly increased responding for sucrose under a progressive ratio schedule of reinforcement.  More specifically, high effort exertion was characterized by increased initiations of reward seeking actions.This effect was dependent on effort  requirements and instrumental contingencies, but was not affected by sucrose pre-feeding.  Together, these findings indicate that VTA DA neuronal activation drives motivational behaviour
by facilitating action initiation. With this study, we show that enhancing excitability of VTA DA neurons is a viable strategy to improve motivational behaviour.

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Is leptin resistance the cause or the consequence of diet-induced obesity?

Kathy C. G. de Git, Céline Peterse, Sanne Beerens, Mieneke C. M. Luijendijk, Geoffrey van der Plasse, Susanne E. la Fleur & Roger A. H. Adan

International Journal of Obesity. Volume 42, pages1445–1457 (2018)

Obesity is strongly associated with leptin resistance. It is unclear whether leptin resistance results from the (over)consumption of energy-dense diets or if reduced leptin sensitivity is also a pre-existing factor in rodent models of diet-induced obesity (DIO). We here tested whether leptin sensitivity on a chow diet predicts subsequent weight gain and leptin sensitivity on a free choice high-fat high-sucrose (fcHFHS) diet.

Based upon individual leptin sensitivity on chow diet, rats were grouped in leptin sensitive (LS, n = 22) and leptin resistant (LR, n = 19) rats (P = 0.000), and the development of DIO on a fcHFHS diet was compared. The time-course of leptin sensitivity was measured over weeks in individual rats. Both on a chow and a fcHFHS diet, high variability in leptin sensitivity was observed between rats, but not over time per individual rat. Exposure to the fcHFHS diet revealed that LR rats were more prone to develop DIO (P = 0.013), which was independent of caloric intake (p ≥ 0.320) and the development of diet-induced leptin resistance (P = 0.769). Reduced leptin sensitivity in LR compared with LS rats before fcHFHS diet exposure, was associated with reduced leptin-induced phosphorylated signal transducer and activator of transcription 3 (pSTAT3) levels in the dorsomedial and ventromedial hypothalamus (P ≤ 0.049), but not the arcuate nucleus (P = 0.558).


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Do humans still forage in an obesogenic environment? Mechanisms and implications for weight maintenance

Jeffrey M. Brunstrom, Bobby K. Cheon

Physiology & Behavior Volume 193, Part B, 1 September 2018, Pages 261-267

Many people struggle to control their food intake and bodyweight. This is often interpreted as evidence that humans are generally predisposed to consume food when it is available, because adiposity offered insurance against the threat of starvation in our ancestral environment. In this paper we suggest that modern humans have actually inherited a far broader range of foraging skills that continue to influence our dietary behaviour. To evaluate this idea, we identify three challenges that would need to be addressed to achieve efficient foraging; (1) monitoring the ‘procurement cost’ of foods, (2) determining the energy content of foods, and (3) proactively adapting to perceived food insecurity. In each case, we review evidence drawn from controlled and observational studies of contemporary humans and conclude that psychological mechanisms that address these challenges are conserved. For contemporary humans who live in fast-paced obesogenic environments, this foraging ‘toolkit’ no longer serves the same function to which it was adapted, and in many cases, this leads to an increase in food intake. Understanding these forms of ‘evolutionary mismatch’ is important because it can provide a stronger theoretical basis for informed dietary interventions that leverage fundamental foraging goals rather than work against them.


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Eating less or more - Mindset induced changes in neural correlates of pre-meal planning

Maike A. Hege, Ralf Veit, Jan Krumsiek, Stephanie Kullmann, Martin Heni, Peter J. Rogers, Jeffrey M. Brunstrom, Andreas Fritsche, Hubert Preissl

Appetite 125 (2018) 492-501

Obesity develops due to an imbalance between energy intake and expenditure. Besides the decision about what to eat, daily energy intake might be even more dependent on the decision about the portion size to be consumed. For decisions between different foods, attentional focus is considered to play a key role in the choice selection. In the current study, we investigated the attentional modulation of portion size selection during pre-meal planning. We designed a functional magnetic resonance task in which healthy participants were directed to adopt different mindsets while selecting their portion size for lunch. Compared with a free choice condition, participants reduced their portion sizes when considering
eating for health or pleasure, which was accompanied by increased activity in left prefrontal cortex and left orbitofrontal cortex, respectively. When planning to be full until dinner, participants selected larger portion sizes and showed a trend for increased activity in left insula. These results provide first evidence that also the cognitive process of pre-meal planning is influenced by the attentional focus at the time of choice, which could provide an opportunity for influencing the control of meal size selection by mindset manipulation.

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A predictive, quantitative model of spiking activity and stimulus-secretion coupling in oxytocin neurons.

Jorge, Maícas-Royo , Gareth Leng , Duncan J MacGregor

Endocrinology 159, 1433-1452 (2018)

Oxytocin neurons of the rat hypothalamus project to the posterior pituitary where they secrete their products into the bloodstream. The pattern and quantity of that release depends on the afferent inputs to the neurons, on their intrinsic membrane properties, and on non-linear interactions between spiking activity and exocytosis: a given number of spikes will trigger more secretion when they arrive close together. Here we present a quantitative computational model of oxytocin neurons that can replicate the results of a wide variety of published experiments. The spiking model mimics electrophysiological data of oxytocin cells responding to cholecystokinin (CCK), a peptide produced in the gut after food intake. The secretion model matches results from in vitro experiments on stimulus-secretion coupling in the posterior pituitary. We mimic the plasma clearance of oxytocin with a two-compartment model, replicating the dynamics observed experimentally after infusion and injection of oxytocin. Combining these models, allows us to infer, from measurements of oxytocin in plasma, the spiking activity of the oxytocin neurons that produced that secretion. These inferences we have tested with experimental data on oxytocin secretion and spiking activity in response to intravenous injections of CCK. We show how intrinsic mechanisms of the oxytocin neurons determine this relationship: in particular, we show that the presence of an after-hyperpolarization (AHP) in oxytocin neurons dramatically reduces the variability of their spiking activity, and even more markedly reduces the variability of oxytocin secretion. The AHP thus acts as a filter, protecting the final product of oxytocin cells from noisy fluctuations.

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