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Influence of fetal growth on current body structure and metabolic function

Influence of fetal growth on current body structure and metabolic function
Influence of fetal growth on current body structure and metabolic function

The main purpose of this thesis was to examine the inter-relationship between body structure and metabolic function, and in particular, how fetal growth marked b birth weight may influence this relationship in such a way as to predispose the individual to greater risk of disease in later life.  The central hypothesis that underlies the work reported in this thesis is that the pattern of growth in early life, marked by birth weight, results in structural and functional changes that are evident in adult life, thereby predisposing the individual to an increased risk of obesity, T2DM and CVD.

Adults born wit a lower birth weight appear to be shorter, lighter and have lower lean and muscle mass and grater fat mass in particular in the central region of the body when compared to adults with higher birth weight.  There were differences in body dimensions (both vertically and horizontally) associated with birth weight. The lower birth weight group had shorter leg length and taller trunk and non-limb length when compared to higher birth weight group at the same height. The differences in body composition associated with birth weight could not be simple explained by the observed differences in body dimensions between groups.  In addition, adult with a lower birth weight have lower energy metabolism in both the fasted and fed state.  These differences in energy metabolism were independent of body size and composition (lean mass).  This implies that metabolic function in itself might be programmed, an effect greater than that simply explained by differences in size and composition.  This less prudent metabolic phenotype associated with differences in birth weight may predispose to more obvious features such as adiposity and central fat which, in turn, may increase the risk of developing T2DM and CVD.

University of Southampton
Kensara, Osama Adnan
14ef0cd0-9cba-4d9b-b2e8-d57242f9abee
Kensara, Osama Adnan
14ef0cd0-9cba-4d9b-b2e8-d57242f9abee

Kensara, Osama Adnan (2006) Influence of fetal growth on current body structure and metabolic function. University of Southampton, Doctoral Thesis.

Record type: Thesis (Doctoral)

Abstract

The main purpose of this thesis was to examine the inter-relationship between body structure and metabolic function, and in particular, how fetal growth marked b birth weight may influence this relationship in such a way as to predispose the individual to greater risk of disease in later life.  The central hypothesis that underlies the work reported in this thesis is that the pattern of growth in early life, marked by birth weight, results in structural and functional changes that are evident in adult life, thereby predisposing the individual to an increased risk of obesity, T2DM and CVD.

Adults born wit a lower birth weight appear to be shorter, lighter and have lower lean and muscle mass and grater fat mass in particular in the central region of the body when compared to adults with higher birth weight.  There were differences in body dimensions (both vertically and horizontally) associated with birth weight. The lower birth weight group had shorter leg length and taller trunk and non-limb length when compared to higher birth weight group at the same height. The differences in body composition associated with birth weight could not be simple explained by the observed differences in body dimensions between groups.  In addition, adult with a lower birth weight have lower energy metabolism in both the fasted and fed state.  These differences in energy metabolism were independent of body size and composition (lean mass).  This implies that metabolic function in itself might be programmed, an effect greater than that simply explained by differences in size and composition.  This less prudent metabolic phenotype associated with differences in birth weight may predispose to more obvious features such as adiposity and central fat which, in turn, may increase the risk of developing T2DM and CVD.

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Published date: 2006

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Local EPrints ID: 466131
URI: http://eprints.soton.ac.uk/id/eprint/466131
PURE UUID: af8551a2-6222-4d3b-9a06-30f1bd113730

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Date deposited: 05 Jul 2022 04:26
Last modified: 16 Mar 2024 20:31

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Author: Osama Adnan Kensara

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