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Dr Caroline Ann Steele, Mbchb, MRCPCH (UK)

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Dr Caroline Ann Steele, Mbchb, MRCPCH (UK) EATING BEHAVIOUR AND NEURAL REPRESENTATIONS OF HUNGER AND SATIETY IN PATIENTS WITH ACQUIRED STRUCTURAL HYPOTHALAMIC DAMAGE: A CLINICAL AND FUNCTIONAL NEUROIMAGING STUDY Thesis submitted in accordance with the requirements of the University of Liverpool for the degree of Doctor of Philosophy by Dr Caroline Ann Steele, MBChB, MRCPCH (UK) December 2017 Institute of Ageing and Chronic Disease, Department of Obesity and Endocrinology, Clinical Sciences Centre, Aintree University Hospital, Liverpool, L9 7AL 1 CONTENTS Page Declaration 4 Abbreviations 5 Abstract 8 Acknowledgements 11 Chapter One Introduction 12 Section I: 13 Section II: 15 Section III: 18 Section IV: 21 Section V: 37 Section VI: 43 Section VII: 44 Section VIII: 54 Section IX (Contribution of thesis to knowledge): 60 Section X: 63 Section XI: 75 Aims of thesis and hypotheses: 94 Chapter Two Methods 96 Chapter Three Adults with acquired structural hypothalamic damage: 103 A 7-year follow-up study 2 CONTENTS PAGE Chapter Four Pituitary tumours in children and adolescents: 124 presentation and long-term endocrine and metabolic outcomes Chapter Five Cerebral activations during viewing of food stimuli in 139 adult patients with acquired structural hypothalamic damage: A functional neuroimaging study Chapter Six Microstructure and macrostructure of eating behaviour 178 in adult patients with acquired, structural hypothalamic damage: a laboratory study of eating rate, total intake and within meal appetite ratings and a real-world assessment of eating behaviour and food intake Chapter Seven Final discussion and future research 222 Chapter Eight Publications and abstracts 234 Appendices 237 References 288 3 Declaration Candidate Dr C A Steele This thesis is the result of work performed whilst registered as a candidate for the degree of Doctor of Philosophy at the University of Liverpool. I declare that no portion of the work in this thesis has been submitted elsewhere for another degree or qualification in any other university or higher institute of learning. This thesis is the result of my own work, with help and support in certain aspects as noted: Dr Joanne Powell-Greig - Completion of final expert analysis of the fMRI data (including the initial statistical analysis undertaken using the fMRI data) and help with interpreting this Professor Jason Halford and Dr Joanne Harrold - Expert guidance on the experimental design of the fMRI and eating behaviour studies Dr Una Masic - Completion of final expert analysis of the UEM data and help with interpreting this Miss Silvia Cicconi – Statistical advice including transformation of data where necessary and initial computation of some of the two-way ANOVAs undertaken and other statistical calculations Research supervisors Dr Christina Daousi Prof. J P H Wilding Prof. Andrej Stancak 4 List of abbreviations 3.0T 3.0 Tesla -MSH -melanocyte-stimulating hormone ACTH Adrenocorticotropic hormone AgRP Agouti-related peptide al Anterolateral am Anteromedial ANOVA One way analysis of variance AO Adult-onset ACC Anterior Cingulate Cortex ARC Arcuate nucleus AUC Area under the curve BDNF Brain-derived neurotrophic factor BMD Bone mineral density BMI Body mass index BMR Basal metabolic rate BOLD Blood-oxygen-level-dependent CART Cocaine- and amphetamine-related transcript CI Confidence interval CRH Corticotrophin-releasing hormone CO Childhood-onset CP Craniopharyngioma CPAP Continuous positive airways pressure cpm Counts per minute DI Diabetes insipidus dl Dorsolateral dm Dorsomedial EE Energy expenditure ELISA Enzyme-linked immunosorbent assay EPI Echo-planar imaging FDR False discovery rate fMRI Functional magnetic resonance imaging fT4 Free thyroxine 5 FWHM Full-width half maximum GLP-1 Glucagon-Like Peptide-1 GH Growth hormone GHD Growth hormone deficiency Gy Gray HO Hypothalamic obesity HOMA-IR Homeostasis model assessment of insulin resistance HV Height velocity HVA Homovanillic acid IGF-1 Insulin-like growth factor 1 IGF-BP3 Insulin-like growth factor binding protein 3 IQR Inter-quartile range LAGB Laparoscopic adjustable gastric banding LH Lateral hypothalamus l-/m- Lateral/medial MC4R Melanocortin-4 receptor MCH Melanin concentrating hormone MDEFT Modified Driven Equilibrium Fourier Transform MNI Montreal Neurological Institute MRI Magnetic resonance imaging NAFLD Non-alcoholic fatty liver disease NFPA Non-functioning pituitary adenoma NPY Neuropeptide Y NTRK2 Neurotrophic tyrosine kinase receptor type 2 OFC Orbitofrontal cortex OGTT Oral glucose tolerance test OR Odds ratio OSA Obstructive sleep apnoea PFC Pre-frontal cortex POMC Pro-opiomelanocorticotropin PVN Paraventricular nuclei PWS Prader-Willi syndrome PYY Peptide-YY 6 QoL Quality of Life QoL-AGHDA Quality of Life Acquired Growth Hormone Deficiency Assessment QUICKI Quantitative Insulin Sensitivity Check Index rCBF Regional cerebral blood flow ROI Region of interest RR Relative risk RTx Radiotherapy SD Standard deviation SE Standard error SMR Standardised mortality rate SO Simple obese/obesity SPM8 Statistical parametric mapping T2DM Type 2 diabetes mellitus TBI Traumatic brain injury TSH Thyroid-stimulating hormone UEM Universal eating monitor VAS Visual analogue scale VFD Visual field defects/deficits vl/vm Ventrolateral/ventromedial VMA Vanillylmandelic acid VMH Ventromedial hypothalamus VTA Ventral tegmental area WHR Waist-to-hip ratio yr Year 7 Abstract Eating behaviour and neural representations of hunger and satiety in patients with acquired structural hypothalamic damage: A clinical and functional neuroimaging study Dr Caroline Anne Steele Hypothalamic obesity (HO) is a relatively rare cause of obesity within the population as a whole, but studies of patients with hypothalamic damage show there is a significant prevalence of obesity within the patient group. Additionally, the obesity is difficult to prevent and manage and increases morbidity and mortality in an already at risk patient group. The work of this thesis had two main objectives. Firstly, to examine the prevalence of obesity and associated morbidities in patients with acquired, structural hypothalamic damage with a descriptive cohort study (n=110). A separate descriptive study quantified obesity and metabolic risk factors in young patients with pituitary tumours, with or without hypothalamic damage (n=41), as they were also identified as a possible at risk group during clinical observations. The second objective was to investigate the underlying pathophysiology of HO using various complementary techniques to study patients with hypothalamic damage who remained weight-stable (HWS), patients with HO and age- and BMI-matched controls. These cross-sectional case-control studies used functional magnetic resonance imaging (fMRI; 9 HO, 7 HWS, 20 controls), the universal eating monitor (UEM; 6 HO, 6 HWS, 9 obese controls [OC], 10 non-obese controls [NOC]), Three-Factor Eating Questionnaire (TFEQ; 8 HO, 6 HWS, 9 OC, 11 NOC) and three-day food diaries (6 HO, 7 HWS, 8 OC, 11 NOC) to assess eating behaviour. The first descriptive study included 110 adults with tumours causing hypothalamic damage attending a specialist neuroendocrine clinic. There was a significant prevalence of weight gain and obesity; 81.8% were overweight/heavier, 56.4% obese and 13.6% morbidly obese, despite proactive assessment and treatment during routine clinic visits. Hypertension (30.9%), dyslipidaemia (54.5%), type 2 8 diabetes mellitus (T2DM) (14.5%) and cardiovascular disease (9.1%) were also prevalent. In 41 patients with childhood/adolescent-onset pituitary adenomas there was also a relatively high prevalence of obesity (39.0%) and cardiovascular risk factors (2 receiving antihypertensive medications, 2 with T2DM and 4 with treated dyslipidaemia), despite the majority of tumours being microadenomas (i.e. too small to cause hypothalamic damage and indicating the need for long-term follow-up of these patients. The first study into the pathophysiology of HO involved the use of functional MRI in 9 patients with HO, 7 HWS and 20 age- and BMI-matched controls. Participants underwent fMRI scans in a fasted state, as well as one hour and three hours following a fixed-load breakfast (25% of their calculated basal metabolic rate [BMR]). At each scan session participants viewed alternating blocks of photographs of high- or low-calorie food, with non-food photographs also viewed to use as a baseline comparison, to allow purely visual activation to be subtracted from any BOLD signal differences which occurred. Whole-brain statistical analysis revealed significantly lower BOLD signal in HWS participants compared to HO (and to controls) in the food motivation and reward-related brain regions of the posterior insula and lingual gyrus (p=0.001) when viewing high-calorie food photographs (compared to non-food photographs). These differences in reward-related brain regions may be implicated in the development of HO/the ability to remain weight- stable despite hypothalamic damage. Eating behaviour studies were undertaken on a separate study day where participants were asked to eat an unlimited pasta meal until adequately full, while seated at the UEM. This allowed monitoring of total intake, eating duration, eating rate and intra-meal on-screen ratings of hunger, fullness and meal pleasantness using visual analogue scales. Additionally Three Factor Eating Questionnaires (TFEQs) and three-day MRC-Human Nutrition Research diaries were completed at home to assess more long-term real-world eating habits. None of the eating behaviour studies identified significant
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