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Title: Body composition and metabolic profile of children with end stage liver disease
Author: Kyrana, Eirini
ISNI:       0000 0004 6497 5886
Awarding Body: King's College London
Current Institution: King's College London (University of London)
Date of Award: 2017
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Children with end stage liver disease are thought to have reduced lean mass and higher energy requirements. The aim of the study was to assess how body composition and energy requirements of children with end stage liver disease differ from those of healthy children and how they change after liver transplantation as well as to study for metabolic pathways that may be influencing the body composition. Body composition was assessed by various methods including basic anthropometry, stable isotopes, dual-energy X-ray absorptiometry (DXA) and air displacement plethysmography (BOD POD). Resting energy expenditure was assessed by indirect calorimetry. The patients were compared to age and sex matched healthy controls and were re-assessed at least 6 months after they received their liver transplant. Liver, muscle and fat tissue obtained at the time of transplant was assessed by microarray analysis of gene expression and validated with qPCR with a focus on metabolic pathways of glycolysis, lipolysis, insulin resistance and muscle atrophy and in particular the AMPK pathway (a cellular catabolic pathway). Seventeen patients and 14 healthy controls were recruited. Basic anthropometry showed that the patients had significantly lower weight and height. The deuterium, BOD POD and DXA measurements showed that whereas some children had lower lean mass, fat mass (FM) was preserved and remained within the normal range. Body mass index, mid upper arm circumference and FM indices were negatively correlated with stay in hospital post liver transplant. The presence of hypermetabolism was not different between patients and controls. The tissue studies distinguished a subgroup of patients with significant differences in their muscle and fat tissue. These differences were not related to catabolic pathways including AMPK, but were related to a pathway linked to inflammatory mediated insulin resistance involving interleukin-6. In this cohort of patients, in spite of lean mass reduction, fat mass was preserved and correlated with a shorter stay in hospital after liver transplantation. This is relevant information when deciding on appropriate nutritional management prior to transplantation. Some patients may develop insulin resistance as a mechanism of fat mass preservation during their chronic illness. This is the first time a possible mechanism for the insulin resistance described in these patients is identified. Further work would be required to confirm this finding and to link it with clinical evidence of insulin resistance.
Supervisor: Dhawan, Anil ; Mitry, Ragai Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available