Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.600111
Title: Modelling and mechanisms of binge eating and diet-induced obesity
Author: Bake, Tina
ISNI:       0000 0004 5350 0746
Awarding Body: University of Aberdeen
Current Institution: University of Aberdeen
Date of Award: 2014
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Abstract:
The studies in this thesis aimed to develop and characterise a rodent model of meal feeding that would mimic aspects of human eating behaviour, leading to the overconsumption of calories and ultimately to obesity. In seeking to identify potential mechanisms that might be involved in the initiation of meals, a palatable scheduled feeding regime was utilised to induce a substantial food intake over short periods of time in rodents. This was done by providing scheduled access to a palatable diet for a 2h-period each day without imposed caloric restriction during the remainder of the day. Initially, the effects of different palatable diets were examined. Three of the four palatable diets resulted in a rapid adaptation of feeding behaviour and induced the consumption of large, binge-type meals in both Sprague Dawley rats and C57BL/6 mice. Candidate gene expression analysis by in-situ hybridisation during the two hour period leading up to scheduled feeding suggested that homeostatic neuropeptide systems in the hypothalamus did not have a major role in driving the consumption of these meals. Further characterisation of the scheduled feeding model revealed that palatable scheduled feeding does not lead to a relative hypophagic phase or an increase in pre-meal secreted gut hormones in anticipation of the scheduled meals. Interestingly, schedule-fed animals exhibited food anticipatory activity during the same period. In addition, scheduled-fed animals displayed only a mild obese phenotype but their metabolic health was adversely affected. Again using in-situ hybridisation, candidate gene expression was assessed during the scheduled feeding period itself, revealing a relationship with adiposity level but not with immediate feeding behaviour. Finally, in a ‘hypothesis-free' approach, gene expression was analysed by microarray at the point of initiation of scheduled feeding, with no apparent changes in gene expression levels. In conclusion, palatable scheduled feeding in mice and rats induces large, binge-type meals that appear not to be directly regulated by homeostatic neuropeptides in the hypothalamus. Investigations into forebrain candidate gene expression by in-situ hybridisation suggested that measuring mRNA levels might not be the optimal analytical approach to demonstrate an involvement of the reward-related signalling system. Alternative strategies for identifying meal feeding mechanisms in the palatable scheduled feeding model could focus on approaches such as neurotransmitter release.
Supervisor: Not available Sponsor: Biotechnology and Biological Sciences Research Council (BBSRC) ; AstraZeneca UK ; British Society of Neuroendocrinology
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.600111  DOI: Not available
Keywords: Compulsive eating ; Obesity
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