Hunger and Satiety Mechanisms and Their Potential Exploitation in the Regulation of Food Intake

Acknowledgments Tehmina Amin is the Project Manager and Julian Mercer is Project Coordinator for Full4Health. Both are funded by the Full4Health project (grant agreement no. 266408) under the EU Seventh Framework Programme (FP7/2007–2013). Julian Mercer is funded by the Scottish Government, Rural and Environment Science and Analytical Services Division, Food, Land and People programme. He is also a partner in FP7 projects: NeuroFAST (grant agreement no. 245099) and SATIN (grant agreement no. 289800).Peer reviewedPublisher PD

Diet-Regulated Anxiety

Peer reviewedPublisher PD

Hypothalamic gene expression during voluntary hypophagia in the Sprague-Dawley rat on withdrawal of the palatable liquid diet, Ensure

Copyright © 2014 Elsevier Inc. All rights reserved.Peer reviewedPostprin

Preclinical models for obesity research

Acknowledgements The authors are funded by the Scottish Government, Rural and Environment Science and Analytical Services Division, Strategic Research Programme, ‘Food, Health and Wellbeing’ Theme. P.B. also acknowledges funding from Biotechnology and Biological Sciences Research Council (BBSRC; BB/M001504/1), J.G.M. from the European Union (EU)-funded Full4Health project (grant agreement no. 266408; Seventh Framework Programme [FP7/2007-2013]), and P.J.M. from BBSRC (BB/G014272/1).Peer reviewedPublisher PD

Getting science to the citizen : 'food addiction' at the British Science Festival as a case study of interactive public engagement with high profile scientific controversy

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Fat, carbohydrate and protein by oral gavage in the rat can be equally effective for satiation

This work was funded by the European Union Seventh Framework programme (Full4Health - grant number 266408) and the Scottish Government Rural and Environment Science and Analytical Services Division to the Rowett Institute. Funders had no role in the preparation of data or the manuscriptPeer reviewedPostprin

Ingestion of Carbohydrate-Rich Supplements during Gestation Programs Insulin and Leptin Resistance but not Body Weight Gain in Adult Rat Offspring

Prenatal nutritional conditions can predispose to development of obesity and metabolic syndrome in adulthood. Gestation with its important modifications in hormonal status is a period of changes in normal feeding habits with pulses of consumption or avoidance of certain categories of food. We tried to mimic in an animal model some changes in food consumption patterns observed in pregnant women. For this purpose, Long–Evans female rats were fed during the dark period, their usual pre-gestational food quantity, and were allowed to complete their daily intake with either a restricted control (Cr), high-fat (HF), or high-carbohydrate (HC) diet available ad libitum during the light period. Dams fed a control diet ad libitum (Ca) served as controls. Body weight and composition, food intake, and metabolic hormones (insulin, leptin) were recorded in male offspring until 20 weeks after birth. Cr and HC females ate less than Ca females (−16%; p < 0.001) and their offspring presented a weight deficit from birth until 6 (HC group) and 10 (Cr group) weeks of age (p < 0.05 or less). Plasma leptin corresponded to low body weight in Cr offspring, but was increased in HC offspring that in addition, had increased plasma insulin, blood glucose, and subcutaneous adipose tissue mass. HF dams ate more than Ca dams (+13%; p < 0.001), but plasma leptin and insulin were similar in their offspring. Hypothalamic Ob-Rb expression was increased in Cr, HC, and HF offspring (+33–100% vs Ca; p < 0.05 or less). HC supplement ingestion during gestation therefore leads to insulin and leptin resistance in adult offspring independently of lower birth weight. These hormonal changes characterize obesity-prone animals. We therefore suggest that attention should be paid to the carbohydrate snacking and overall carbohydrate content in the diet during the last weeks (or months) preceding delivery to limit development of later metabolic disorders in offspring

A spontaneous binge-like eating model in mice using unpredictable once weekly access to palatable diets

The authors are grateful for funding from the Scottish Government Strategic Research Programme, and from the European Union Seventh Framework Programme (FP7/2007-2013) under grant agreement 245009 (NeuroFAST).Peer reviewedPostprin

Body weight loss, effective satiation and absence of homeostatic neuropeptide compensation in male Sprague Dawley rats schedule fed a protein crosslinked diet

Acknowledgements This work was funded by the European Union Seventh Framework programme (Full4Health - grant number 266408) and the Scottish Government Rural and Environment Science and Analytical Services Division. We thank Danisco, Kettering, UK, for the gift of emulsifier. We thanks Dr Claus-Dieter Mayer of Biomathematics & Statistics Scotland for help with statistical analysis.Peer reviewedPostprin

Hypothalamic ventricular ependymal thyroid hormone deiodinases are an important element of circannual timing in the siberian hamster (Phodopus sungorus)

Exposure to short days (SD) induces profound changes in the physiology and behaviour of Siberian hamsters, including gonadal regression and up to 30% loss in body weight. In a continuous SD environment after approximately 20 weeks, Siberian hamsters spontaneously revert to a long day (LD) phenotype, a phenomenon referred to as the photorefractory response. Previously we have identified a number of genes that are regulated by short photoperiod in the neuropil and ventricular ependymal (VE) cells of the hypothalamus, although their importance and contribution to photoperiod induced physiology is unclear. In this refractory model we hypothesised that the return to LD physiology involves reversal of SD expression levels of key hypothalamic genes to their LD values and thereby implicate genes required for LD physiology. Male Siberian hamsters were kept in either LD or SD for up to 39 weeks during which time SD hamster body weight decreased before increasing, after more than 20 weeks, back to LD values. Brain tissue was collected between 14 and 39 weeks for in situ hybridization to determine hypothalamic gene expression. In VE cells lining the third ventricle, expression of nestin, vimentin, Crbp1 and Gpr50 were down-regulated at 18 weeks in SD photoperiod, but expression was not restored to the LD level in photorefractory hamsters. Dio2, Mct8 and Tsh-r expression were altered by SD photoperiod and were fully restored, or even exceeded values found in LD hamsters in the refractory state. In hypothalamic nuclei, expression of Srif and Mc3r mRNAs was altered at 18 weeks in SD, but were similar to LD expression values in photorefractory hamsters. We conclude that in refractory hamsters not all VE cell functions are required to establish LD physiology. However, thyroid hormone signalling from ependymal cells and reversal of neuronal gene expression appear to be essential for the SD refractory response